Dr Francis FC IP

COMMON PAEDIATRIC DERMATOLOGICAL PROBLEMS: AN UPDATE

NO CONFLICT OF INTEREST RELATED TO THIS TALK

Common Paediatric Dermatological Problems

• Jan - July 2015

• 322 paediatric dermatology new referrals seen in DH YFS Dermatological Clinic (13.4% of total new referrals)

• Total new referrals 2393

•Referral sources:

•public sector approx. 70%

•private sector approx. 30%

Common Paediatric Dermatological Problems

35.4%

18.0%

11.2%

7.1%

2.8%

0.00%

5.00%

10.00%

15.00%

20.00%

25.00%

30.00%

35.00%

40.00%

Atopic Dermatitis

(n=114)

Wart (n=58) Naevus (n=36) Acne (n=23) Birthmark (n=9)

% of New Cases

Common Paediatric Dermatological Problems • Top five referring diagnosis:

• 1. Atopic dermatitis (35.4%)

• 2. Wart (18.0%)

• 3. Naevus (11.2%)

• 4. Acne (7.1%%)

• 5. Birthmark (2.8%)

• Other common referring diagnoses are: Alopecia areata, Molluscum contagiosum, pigmentary disorders, seborrhoeic dermatitis, psoriasis, chronic urticaria, keratosis pilaris, milia etc.

Common Paediatric Dermatological Problems • Most paediatric skin referrals are from general outpatient clinic,

student health service, MCH, GPs

• Patients with warts, birthmark, acute dermatological conditions, worrying nevi are referred early

• Provisional diagnosis are given in referral >90%

• Most paediatric patients are accompanied by parent(s), but some are accompanied by domestic helpers, grandparents or other relatives

• Pitfalls:

• Difficult to explain treatment plans and conduct health education

• Compliance problem

• Conflicts between caretakers

COMMON WART

Common Wart: Facts • Infection of keratinocytes by HPV: double-stranded

DNA virus

•Common warts on hands and feet: HPV type 1, 2, 4, 27, 57

•Plane warts: HPV type 3 and 10

• Infection by multiple types common

•Viral activity depends on immune status and response

•Recurrence after clinical remission: reactivation or reinfection

Common Wart: Facts • Mode of transmission:

• Direct person to person contacts

• Indirect contacts

• Autoinoculation

• Up to 10% affected in general population, peak age 12-16yrs

• In children approx. 1/3 clear spontaneously within 3 months, ½ clear at 1 year and >2/3 clear up by 2 years

• Adults are much slower in self-clearance

• Previously infected have higher risk for new warts development

• Clearance rate affected by viral type, host immune response, extent and duration of warts

Common Wart • Clinical diagnosis: usually adequate

• Paring, dermatoscope, biopsy

• DDx: callosities, corn, seborrhoeic keratosis, actinic keratosis, focal PPK, LP

• Different clinical forms

• Verruca vulgaris, plane wart, plantar wart, mosaic wart, filiform wart, periungal wart

• Treatment

• No cure yet

• Does not alter transmissibility

• Control symptoms and signs

• No single treatment is completely effective

• Combination treatment sometimes required

Common Wart • Treatment

• Expectant

• Destructive therapy

• Salicylic acidA, cryotherapyB, curettageD, cauteryD, excisionD, CantharidinD

• LasersC: CO2 laser, Er:YAG laser, Nd:YAG laser, PDL, KTP laser

• Photodynamic therapyD

• Anti-viral therapy

• GlutaraldehydeD, formaldehydeD, cidofovirD

• Anti-mitotic therapy

• BleomycinC, podophyllinD, podophyllotoxinD, systemic retinoidD, 5-FUC

• Immunotherapy

• Contact sensitizerC, imiquimodD, TCAAD, phenolD, Vit D analoguesD

Sterling et al. BJD 2014

Common Wart • Alternative therapy: insufficient evidence

• Dithranol

• Formic acid

• H2 receptor antagonists: cimetidine, ranitidine

• Herbal treatment: e.g. garlic, fig sap

• Homeopathy

• Hypnotherapy

• Intralesional immunotherapy

• Occlusive therapy (e.g. duct tape)

• Retinoids, topical

• Silver nitrate

• Zinc oxide

• Zinc sulfate

Common Wart • Pearls

• Pre-treatment to reduce thickness of wart recommended whenever possible

• Combination treatment may be beneficial

• Treatment in children requires careful consideration especially with painful treatment in small children

• Topical salicylic acid probably the best choice in children: ?optimal concentration, ?use under occlusion

• Future

• Trials for glutaraldehyde and formaldehyde

• Trials for Vit D analogues

• Trials for AgNO3, Cantharidin, TCAA, phenol

• Trials for immunotherapy

• Vaccines

ATOPIC DERMATITIS

Atopic dermatitis

•Atopic dermatitis / Atopic eczema: • Chronic pruritic inflammatory skin disease that had a relapsing

course and occurs most frequently in children

• Onset most frequent before 6 months of age

• 60% in the 1st year, 90% by 5 years of age

• Majority had disease resolved by adulthood

• 10-30% had persistent disease into adulthood

• Complex interplay between genetic, immunologic and environmental factors

• Dx mostly clinical

Atopic Dermatitis Diagnostic criteria

• Essential features

1. Pruritus

2. Eczematous changes:

I Typical and age-specific patterns* II Chronic or relapsing course

*Patterns include: (a) facial, neck, and extensor involvement in infants and children; (b) current or prior flexural lesions – adults/any age; (c) sparing of groin and axillary regions

• Important features (seen in most cases):

1. Early age of onset

2. Atopy (IgE reactivity, personal and/or family history)

3. Xerosis

• Associated features:

• 1 Atypical vascular responses 2 Keratosis pilaris/ichthyosis/palmar hyperlinearity 3 Ocular/periorbital changes 4 Other regional findings (e.g., perioral/periauricular lesions) 5 Perifollicular changes

Hanifin JM Acta Dermato Venereol 1980.

Atopic dermatitis •Pathogenesis:

1. Skin barrier dysfunction

2. Immune dysregulation

• 2 strong risk factors: 1. Family history of atopy

2. Loss of function mutation of FLG gene (Chromosome 1q21)

• 70% AD patients had +ve family Hx of atopy

• 2-3x risk of AD with 1 atopic parent

• 3-5x risk of AD with both parents atopic

• Defective barrier function:

• Skin function as a BARRIER to physical, chemical and biological insult

• Break down of the epidermal barrier: primary event in AD • Stratum corneum: the most important barrier

• An alteration of the barrier causes trans-epidermal water loss: hallmark of AD

• Alteration of intercellular lipids and enzyme involved in adhesion of epidermal keratinocytes

• Filaggrin mutation: Chromosome 1q21, loss of function null mutation cause earlier onset and more severe persistent AD

• Up to 40% with FLG null alleles do not have AD

Pathogenesis

•Defective barrier function 1. Down-regulation of cornified envelope genes:

filaggrin 2. Reduced ceramide levels 3. Increased levels of endogenous proteolytic

enzymes 4. Enhanced trans-epidermal water loss 5. Lack of endogenous protease inhibitors 6. Exogenous proteases from Staphylococcus aureus

and house dust mites 7. Soaps and detergents: change of epidermal pH

Pathogenesis

•Cutaneous inflammation • Inflammation is mediated by a complex expression of cytokines and chemokines.

• Mechanical injury, from trauma, infection, or even scratching production of interleukin 1 (IL-1) and TNFα

• These cytokines bind to vascular endothelium receptors, activate cellular signaling pathways, induce vascular endothelial cell adhesion molecules, and lead to extravasation of inflammatory cells into the skin

• Acute AD: production of T-helper type 2 (Th2) cytokines such as IL-4, IL-13, IL-31 which mediate switching to IgE synthesis and expression of adhesion molecules on endothelial cells. Increased levels of IL-17, a cytokine that induces the release of proinflammatory mediators from macrophages and fibroblasts

• Chronic AD lesions are associated with IL-5, which is involved in eosinophil development and survival, production of the Th1-like cytokines IL-12 and IL-18, and several remodeling-associated cytokines such as IL-11 and transforming growth factor β1

Pathogenesis

MANAGEMENT

Disease control

Clearance

Prevention

Maintenance

Crisis management

•Accurate and early diagnosis

•Tailor-made treatment plan

•Importance of compliance: main reason of treatment failure

•Explore the lifestyle of patient and family, preference and practicability of therapy

Management

Team approach: •Clinic visit: pre-consultation, consultation, post-consultation •Role of primary care physician •Treatment plan •Education information •Dermatologist •Nursing specialist •Follow-up

Planning of treatment

Management

•Clearance: • Topical therapy to achieve total or near total clearance of disease

• To break off the itch-scratching vicious cycle

• Potent topical steroid

• New generation/ lipophilic type, preferably ointment base

• Topical calcineurin inhibitor

• Mainly for facial/ periorbital area

• Concomitant use of emollient

• Modification of topical therapy

• Wet wrap dressing: with diluted steroid or emollient

•Crisis management

• Acute flare up of disease

• Secondary infections

• Eczema herpeticum

• May need in-patient supervised therapy: wet wrap dressing

• Parenteral antibiotics/ antivirals

Management

Management

•Maintenance and prevention:

• Emollient

• Allergen and trigger avoidance

• Pro-active approach with topical steroid

• Life style modification

Management

•Potential triggers

• Associated with direct contact: Toiletries containing alcohol, astringents, or fragrances, harsh detergents/soaps

• Abrasive clothing (wool or synthetics)

• Associated with physiologic/emotional stressors: Infections (especially from S aureus, viruses, fungi, etc.) Overheating/sweating Psychological stress

Management • Topical therapy

1. Moisturizer

2. Bathing and bathing additives

3. Topical corticosteroid

4. Topical calcineurin inhibitor

5. Wet wrap therapy

6. Bleach bath

• Phototherapy

• Systemic therapy

• Adjunctive therapy

Management • Topical therapy

• Moisturizer (level I)

• Bathing (level III)

• Application of moisturizer after bath (level II)

• Wet wrap therapy (level II)

• Topical corticosteroid (level I)

• Topical calcineurin inhibitor (level I)

• Bleach bath and intranasal mupirocin (level II)

• Proactive use of topical corticosteroid (level I)

• Proactive use of topical calcineurin inhibitor (level I)

Eichenfield LF et al. JAAD 2014

Management •Emerging topical therapy

•Boron-based phosphodiesterase 4 (PDE4) inhibitor:

•Crisaborole oint (Phase 3)

•Small molecule PDE4 inhibitor:

•Roflumilast cream (Phase 2)

• Janus kinase inhibitor (IL-4, IL-5, IL-31 pathways):

•Tofacitinib oint (Phase 2)

•Wet Wrap Dressing

• Advocated for AD treatment since 1991

• Used for treatment of severe or refractory atopic dermatitis

• Variation of methodology

• Efficacy overall is good

• Use with topical steroid is more efficacious than emollient alone

Management

Goodyear HM, Spowart J, Harper JI. Br J Dermatol 1991

• Advantages:

1. Wet wraps increase skin hydration

2. Serve as an effective barrier to scratching

3. Helps promote more restful sleep

4. Promotes penetration of topical corticosteroids into the skin, increase amount of medication delivered to the affected areas

5. Use in severe disease or disease refractory to standard topical therapy

Wet Wrap Dressing

• Problems:

1. Time consuming and labor intensive compliance

2. Systemic side effect of topical corticosteroid

3. Discomfort: chills, paradoxical dryness

4. Folliculitis (common), other infective complications (rare)

5. Striae: especially in teenage

Wet Wrap Dressing

1. Topicals: emollient (ointment or cream), topical steroids

2. Bandages

3. Technique of application: direct application to skin (avoid double dip!)

4. Frequency of Tx: once daily

5. Re-wetting

6. Area to treat: extremities, body, face

7. Duration of application: 3, 6-8, 12, 24 hrs (depend on setting); 2-14 days (recommended 7 days)

Wet Wrap Dressing: How to start

• Diluted bleach bath: adjuvant anti-infective treatment • Decrease local skin infections • Reduce the need for systemic antibiotics for patients

with AD heavily colonized and/or superinfected skin • 76-100% of Staphylococcus aureus colonization in AD

patients vs. 2-25% healthy controls • Related to abnormal epidermal barrier: ceramide and

sphingosine def, increase serum protease and decrease filaggrin expression

• Antimicrobial peptides are reduced, because of local production of interleukins

• S aureus superantigens activate keratinocytes, inducing the release of proinflammatory cytokines and exacerbating AD

Bleach Bath

•Bleach shown in-vitro and in-vivo anti-Staph activity (MSSA and MRSA)

•Use of bleach bath and concomitant intranasal mupirocin ointment: improve severity of AD in patients who are prone to infections1

Good tolerance to bleach bath

Do not eradicate S aureus

7.4% CA-MRSA from lesions, 4% from nares

Bleach Bath

Huang JT et al. Pediatrics 2009

• Explain to patients that their skin may benefit from “swimming in pool water.”

• Add lukewarm water to fill the tub. Add bleach solution to the bath water ()

• Final concentration of about 0.005%, ensure that the bleach is completely diluted in the bath water

• Soak for 5 to 10 minutes

• Thoroughly rinse skin clear with lukewarm, fresh water at the end of the bleach bath

• As soon as the bath is over, pat the patient dry. Do not rub dry, immediately apply any prescribed medications/emollients. Repeat bleach baths 2–3 times a week or as prescribed by the physician.

• The following restrictions apply:

1. Do not use undiluted bleach directly on the skin. Even diluted bleach baths can potentially cause dryness and/or irritation

2. Do not use bleach baths if there are many breaks or open areas in the skin (for fear of intense stinging and burning)

3. Do not use bleach baths in patients with a known contact allergy to chlorine

Bleach Bath: How to start

Krakowski AC et al. Pediatrics 2008

Management • Phototherapy (level II)

• Narrow band UVB (most commonly recommended)

• Broad band UVB

• UVA

• Psoralen plus UVA

• Systemic immunomodulating medications (all off-label use)

• Cyclosporine

• Azathioprine

• Methotrexate

• Mycophenolate

• Emerging systemic therapy

• Dupilumab (anti-IL-4 and IL-13)1

• Apremilast (PDE4 inhibitor)2: undergoing phase II

1. Beck et al, NEJM 2014 2. Samrao A et al. Arch Dermatol 2012

Management • Dupilumab (Beck LA et al, NEJM 2014)

• Fully human monoclonal antibody that blocks IL-4 and IL-13, has shown efficacy in patients with asthma

• Monotherapy in two 4-week trials and in one 12-week trial and in combination with topical steroid in another 4-week study

• In 12-week study of dupilumab monotherapy reproduced and extended the 4-week findings: 85% of patients in the dupilumab group, as compared with 35% of those in the placebo group, had a 50% reduction in the EASI score

• In 4-week combination study, 100% of the patients in the dupilumab group, as compared with 50% of those who received topical steroid with placebo injection, achieved EASI-50

• Dupilumab group also use less than half of topical steroid compare to placebo group

Management • Adjunctive therapy

• Structures education program (level I)

• Eczema workshop, nursing program (level II)

• Allergy assessment only if positive history elicited (level II)

• Patch testing for ACD (level II)

• Food elimination based on allergy tests only is not recommended (level II)

• Avoidance if true IgE mediated allergy (level I)

• Insufficient evidence to recommend routine use of probiotic/ prebiotic, fish oils, evening primrose oil, borage oil, Vit. D, E, B12, B6

• Insufficient evidence to sublingual and injectional immunotherapy

Management • Allergy and testings

• Definition of allergy: adverse health event that results from exposure to allergens with reproducibility

• Multiple sensitization in AD patients is common, but not true allergy

• Poor correlation with clinical allergic response in positive allergy testing without a history of reaction to foods

• Exposure to allergenic food often give rise to type I response

• Delayed eczematous response is not clearly defined

• Recommendation in limited allergy testing if either one or both factors are present in a child <5 yrs with moderate to severe AD (test for cow’s milk, egg, soy, wheat, peanut):

1. Persistent severe disease despite optimized treatment

2. A reliable history of immediate allergic reaction after ingestion of a specific food

Management • Allergy testings

• Negative predictive value is high (>95%) for food-specific IgE and SPT, specificity and positive predictive value low (40-60%)1,2,3

• Positive result only signify sensitization, clinical correlation and confirmation test is required to establish presence of allergic disease

• Higher specific IgE level and larger wheal associated with increase likelihood of reaction on challenge

• Atopy patch test: not recommend for routine use

• Gold standard: double-blind placebo-controlled oral food challenge4

• Aeroallergens: pathogenetic role in AD controversial

1. Bock SA et al. Clin Allergy 1978 2. Sampson HA et al. J Allergy Clin Immunol 1984 3. Lemon-Mule H et al. Curr Allergy Asthma Rep 2008 4. Boyce JA et al. J Allergy Clin Immunol 2010

MELANOCYTIC NAEVI

Melanocytic naevi • Congenital melanocytic naevi (CMN)

• Present at birth

• Acquired melanocytic naevi

• Develop after birth

• Clinical appearance and histological presentation differ

• In Caucasian studies, 1-2% newborn developed CMN

• Melanoma developed very rarely before puberty but steadily increase incidence after puberty

• Management is mainly diagnosis and watchful observation

• Sequential photograph, dermoscopy help to diagnose and monitor

• Confocal laser scanning microscopy

Congenital melanocytic naevi • Commonly classified into 3 groups:

• Small CMN: <1.5cm

• Medium CMN: 1.5cm to 19.9cm

• Giant CMN: ≥20cm

Location of CMN Diameter at birth

Head 12cm

Hands, feet, forearm, arm, buttock 7cm

Thighs 5.8cm

Legs 6cm

Marghoob AA et al. Arch Dermatol 1996

Congenital melanocytic naevi •Problems with large/ giant CMN

•Psychosocial issues

•Risk of melanoma

•Neurocutaneous melanosis

•Non-malignant association: most common café-au-lait macules

Congenital melanocytic naevi • Risk of melanoma in CMN

• Increase with size of CMN

• Small and medium CMN

• Likely <1% (general lifetime risk of melanoma in US: 1.97%)

• Giant CMN

• Wide range due to rarity and heterogeneity of giant CMN

• Likely <5%

• Multiple CMN and satellite naevi

• Data limited

Congenital melanocytic naevi • Neurocutaneous melanosis

• Congenital dysmorphogenesis of ectoderm, melanocytic proliferation in leptomeninges and brain parenchyma

• Most presented before 2 years of age

• Incidence 2.5% - 45%

• Risk factors: giant CMN, male, satellite naevi, multiple CMN, head and neck or posterior mid-line location

• MR Imaging controversial in asymptomatic children

Congenital melanocytic naevi • Treatment options: (Only low level of evidence)

• Observation

• Full thickness procedure

• Excision at one stage or serial

• Partial thickness procedure

• Dermatome shaving

• Curettage

• Dermabrasion

• Chemical peels

• Cryotherapy

• Electrosurgery

• Lasers: ablative and pigment-specific

ACNE VULGARIS

Acne vulgaris • Not necessarily disease of teenager

• 12 years of age: no longer lower end of age of onset

• Early onset 9 – 10 years of age1

• Special consideration in neonate, infant, young children

1. Lucky AW et al. Arch Dermatol 1994

Acne type Age of onset

Neonatal Birth to ≤6 wks

Infantile 6 wks to ≤1 yr

Mid-childhood 1 yr to <7 yr

Pre-adolescent ≥7 yr to ≤12 yr or menarche

Adolescent 12 yr to 19 yr or after menarche

Eichenfield LF et al. Pediatrics 2013

Acne vulgaris • Neonatal acne

• May affect up to 20% of newborn

• True comedonal acne very rare

• Due to delayed physiological regression of fetal zone of adrenal gland postnatal

• Mostly are acneiform conditions without comedones

• Neonatal cephalic pustulosis

• Transient neonatal pustular dermatosis

• Folliculitis

• Miliaria rubra

Acne vulgaris •Neonatal cephalic pustulosis

•Normal colonization of Malassezia species

• Inflammatory reaction to overgrowth of yeast at birth

•Mild and self-limiting

•Severe cases: topical antifungal

Acne vulgaris • Infantile acne

• More common in boys

• Begin at or >6 wks of age

• Last for 6 – 12 months

• Comedones and inflammatory papules, pustules or nodules

• May predispose to severe adolescent acne

• Important to look for testicular growth, breast growth, hirsutism or virilization, growth abnormality

• Treatment

• Topical antibiotics

• Non-tetracycline antibiotics orally

• Topical retinoid

• Systemic retinoid

Acne vulgaris • Mid-childhood acne is very rare

• Should investigate for endocrine abnormality

• Preadolescent acne more common with a trend towards earlier adrenarche and menarche

• Typical comedones in T-zone

• Few inflammatory lesions

• Treatment is similar to adolescent acne

Acne vulgaris •Treatment approach

•Reduce sebum production

•Prevent comedone formation

•Reduce Propionibacterium acne

•Reduce inflammation

•Only systemic retinoids targets all 4 mechanisms, while other treatment modalities target one or two mechanisms

Acne vulgaris • Topical therapy

• Benzyl peroxide (BPO): can be used as monotherapy or in combination

• Topical antibiotics: not recommended as monotherapy

• Topical retinoids: can be used as monotherapy or in combination

• Systemic antibiotics

• Not to use tetracycline group in children younger than 8 years

• Second generation tetracyclines preferred

• Use in combination with topical BPO or retinoids

• Isotretinoin

• Recommended for severe, scarring or refractory acne in adolescent

• Low dose vs. high dose

• Cumulative dose 120-150mg/kg

Acne vulgaris • Hormonal therapy

• Suppressing ovarian androgen production and block androgen effect on sebaceous gland

• Combined oral contraceptive as second line therapy in pubertal female with moderate to severe acne

• Topical dapsone

• 5% dapsone gel: most effective in inflammatory lesions

• More effective when combine with topical retinoid

Acne vulgaris • Treatment recommendations

1. Mild acne

• BPO, topical retinoids, topical antibiotics

• Monotherapy or combination therapy

2. Moderate acne

• BPO, topical retinoids, topical antibiotics, oral antibiotics, hormonal therapy

• Combination therapy recommended

3. Severe acne

• Oral antibiotics, topical retinoids, BPO, oral isotretinoin, hormonal therapy

• Combination therapy recommended

Eichenfield LF et al. Pediatrics 2013

BIRTHMARK

Birthmark

• Presence at birth or shortly after birth

• Category:

1. Vascular/ lymphatic (common)

2. Melanocytic (common)

3. Organoid: Sebaceous, follicular, sweat gland etc. (uncommon)

4. Non-organoid: keratinocytic (common)

5. Others: smooth muscle, collagen (rare)

• Ectodermal or mesodermal origin

• Mostly sporadic and non-syndromic

Vascular birthmark • Vascular anomalies classification

• ISSVA consensus 2014 ( )

Vascular anomalies

Vascular tumors

Vascular malformations

Benign Locally aggressive or borderline Malignant

Simple Combined Of major named vessels

Associated with other anomalies

Capillary malformations Lymphatic malformations Venous malformations Arteriovenous malformations Arteriovenous fistula

CVM, CLM LVM, CLVM CAVM CLAVM Others

Lymphatics Veins Arteries

Origin, course, number, length, diameter, valves, communication, persistence of embryonal vessel

Various syndromes

Vascular birthmark • Nevus simplex vs. Port-wine stains

• Both are capillary malformations

• Nevus simplex

• superficial vascular malformation consists of ectatic capillaries that represent persistence of fetal circulatory pattern

• Up to 40% newborn affected

• Usually located in central portion of face, nuchal area, upper eyelids

• 81% on nape of neck, 45% on eyelids, 33% on glabella1

• Facial lesions fade by 1-2 yrs of age

• Nuchal lesions tend to persist into adulthood

• Port-wine stains (Nevus flammeus)

• Up to 0.3% newborn affected2, equal sex distribution

• No spontaneous resolution, grow in proportion with child

1. Leung AK Pediatr Dermatol 1989 2. Jacobs AH Pediatrics 1976

Vascular birthmark • Port-wine stains

• Unilateral and segmental, can occur on any body parts

• 85% unilateral, 15% bilateral, 68% more than one dermatome involved

• Can be bilateral involvement

• 8% of V1 lesion had ocular or CNS involvement

• Increase risk of ocular or CNS involvement to 25% if bilateral V1 dermatome or V1-3 dermatome affected

• Mostly are cosmetic problem, especially facial involvement

• Progressive darkening, thickening and increase nodularity with underlying bony/ soft tissue hyperplasia develop over time

• Pulsed dye laser (585-595nm) remain the main stay of treatment

• Recurrence occur in up to 10% of patients 2-4 yrs after good response treatment

• Unlikely to prevent deeper bony/ soft tissue hypertrophy

Vascular birthmark • Infantile hemangioma (IH) vs. Congenital hemangioma (CH)

• IH much more common than CH

• IH: GLUT-1 +ve, appear after birth

• Prevalence: Australia 2.6%1, USA 4.5%2

• Non-Hispanic white, F:M=3:1

• Head and neck predilection up to 60%, trunk 25% and extremities 15%

• Spontaneous involution

• CH: GLUT-1 –ve, present at birth

• Congenital hemangioma (CH)3,4: in-utero growth phase and presented full size at birth, no further postnatal growth

• Non-involuting congenital hemangioma (NICH)

• Rapidly involuting congenital hemangioma (RICH)

• Partially involuting congenital hemangioma (PICH)

• M:F = 1:1, predilection to craniofacial area or limbs

1. Dickison et al. Pediatr Dermtol 2011 2. Kanada et al. J Pediatr 2012 3. Boon LM et al. J Pediatr 1996 4. Krol A et al. Arch Facial Plast Surg 2005

Congenital hemangioma

Size

Age

Growth curve of hemangiomas

NICH

RICH

IH

1. Mulliken JB et al. JAAD 2004

Acknowledgement • Dr Ben TH Chan

• YFS Dermatological Clinic Nursing Team