Skin Condition Hub

A

Aesthetic / dermal-managedInflammatory · Pilosebaceous

Acne vulgaris

A chronic inflammatory disease of the pilosebaceous unit presenting as comedones, papules, pustules, nodules and, in severe cases, scarring. One of the most common presentations in aesthetic practice and a frequent driver of post-inflammatory pigmentation.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

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Capture comedonal, inflammatory (papulopustular) and nodulocystic/scarring examples for the three slots. · Reference image search: Wikimedia · Open-i

Primary causes

Follicular hyperkeratinisation — abnormal keratinocyte shedding obstructs the follicle.
Increased sebum production driven by androgens (puberty, hormonal fluctuation, PCOS).
Cutibacterium acnes proliferation in the obstructed, sebum-rich follicle.
Inflammation — immune response to C. acnes and follicular rupture.
Contributing factors: genetics, high-glycaemic diet, comedogenic products, occlusion, some medications.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Benzoyl peroxide	Antimicrobial / comedolytic; first-line, no resistance	OTC / TGA
Adapalene	Topical retinoid — comedolytic, anti-inflammatory; pairs with BPO	TGA
Azelaic acid 15–20%	Comedolytic, antibacterial, anti-pigment; pregnancy-safe	TGA
Clindamycin (topical)	Topical antibiotic — only with BPO, never monotherapy	Script
Clascoterone 1% (Winlevi)	Topical androgen-receptor inhibitor; TGA-registered 2024	Script
Doxycycline / minocycline	Oral antibiotic, moderate–severe; time-limited	Script
Isotretinoin	Oral retinoid — severe/scarring/refractory; specialist, teratogenic	Specialist
COCP / spironolactone	Hormonal — adult-female / hormonal-pattern acne	Script

Treatment modalities to investigate

LED phototherapy — blue (~415 nm) targets C. acnes; red (~633 nm) anti-inflammatory; combined outperforms either alone, all Fitzpatrick types, no thermal risk.
Topical niacinamide (vitamin B3) 4–5% — reduces sebum and inflammation; comparable to topical clindamycin without resistance.
Salicylic / mandelic acid peels — lipophilic exfoliation; mandelic gentler in darker skin.
Professional extractions for comedonal load.
Post-inflammatory pigment — azelaic acid, niacinamide, vitamin C, strict photoprotection.

Cautions & contraindications

Isotretinoin and procedures — avoid fully ablative laser and mechanical dermabrasion during and ~6 months after; document any elective resurfacing decision.
Pregnancy — topical retinoids contraindicated; azelaic acid preferred. Isotretinoin is teratogenic.
Antibiotic stewardship — never antibiotic monotherapy; always pair with BPO and limit duration.
Photosensitisers (doxycycline, retinoids) — reinforce daily SPF, especially before light-based treatment.

Practitioner review — Acne vulgaris

A

Recognise & referPre-malignant · Keratinocytic

Actinic keratosis

Actinic keratosis (solar keratosis)

A pre-malignant, rough, scaly lesion on chronically sun-exposed skin — a marker of field cancerisation and a recognised precursor to squamous cell carcinoma. Common in the older Australian population. Recognise and refer, do not treat cosmetically.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

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Solitary lesion, multi-lesion field damage, and a 'suspicious change' example. · Reference image search: Wikimedia · Open-i · NCI Visuals Online

Primary causes

Cumulative UV radiation — chronic sun exposure driving keratinocyte DNA damage.
Fair skin (Fitzpatrick I–II) and older age.
Immunosuppression — notably organ-transplant recipients.
Field cancerisation — diffuse sun damage across a region.

Recognise & refer

Actinic keratosis sits on the pathway to squamous cell carcinoma. Cosmetic resurfacing over an unassessed lesion risks masking or delaying a skin-cancer diagnosis. Recognise, counsel on photoprotection, and refer for diagnosis and field management.

Clinically proven treatments (medically directed)

Agent	Class / clinical use	Status
Cryotherapy	Solitary, discrete lesions; medically performed	Medical
5-Fluorouracil cream	Field therapy — highest cumulative clearance	Script
Imiquimod	Field therapy — immune-mediated	Script
Photodynamic therapy	Field therapy — daylight or conventional	Medical
Diclofenac / nicotinamide	Adjunct / chemoprevention in selected patients	Medical

Clinical approach & referral

Recognition and referral is the practitioner role, not cosmetic treatment.
Photoprotection counselling — rigorous daily SPF as the key long-term measure.
Field management is medically directed — GP, skin-cancer clinic or dermatologist.
Follow-up — review 3–6 months after treatment; persistent/suspicious lesions biopsied.

Cautions & contraindications

Do not perform cosmetic resurfacing, peels or laser over a suspected AK before medical assessment.
Urgent referral for any lesion thickening, tender, bleeding, ulcerating or rapidly changing — exclude SCC.
Field-damaged skin signals high lifetime skin-cancer risk — advise full skin checks.
No field therapy is PBS-subsidised in Australia — relevant to cost discussions.

Practitioner review — Actinic keratosis

A

Aesthetic / dermal-managedKnow when to referHair · Androgen-driven

Androgenetic alopecia

Androgenetic alopecia (pattern hair loss)

Progressive, patterned hair thinning — frontal/vertex in men, diffuse crown widening in women — driven by genetic sensitivity to androgens. Common, treatable early, but other causes of hair loss must be excluded first.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

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De-identified crown/part-line views; avoid identifiable full-face images. · Reference image search: Wikimedia · Open-i

Primary causes

Genetic androgen sensitivity — follicular miniaturisation via dihydrotestosterone (DHT).
Hormonal factors — androgen excess, PCOS in women.
Age — prevalence and severity increase over time.
Aggravators / mimics to exclude: thyroid disease, iron deficiency, telogen effluvium, alopecia areata.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Minoxidil (topical)	Prolongs anagen; first-line, men and women	OTC / TGA
Finasteride	Oral 5-alpha-reductase inhibitor (men)	Script
Spironolactone	Anti-androgen for female pattern loss	Script
Low-dose oral minoxidil	Emerging prescriber-led option	Script (off-label)

Treatment modalities to investigate

Low-level laser / LED therapy (red light) — modest evidence for density.
Platelet-rich plasma (PRP) — adjunct with growing evidence.
Microneedling as a delivery adjunct to topical minoxidil.
Nutritional review — correct iron, vitamin D, thyroid where deficient.

Cautions & contraindications

Exclude other causes first — sudden, patchy or scarring loss warrants referral, not cosmetic treatment.
Finasteride — teratogenic risk; not for women of childbearing potential; counsel on sexual side effects.
Set expectations — treatment slows/stabilises loss; results take months and require maintenance.
Scarring alopecia (redness, scaling, follicle loss) — refer to dermatology promptly.

Practitioner review — Androgenetic alopecia

A

Aesthetic / dermal-managedVascular · Benign

Cherry angioma

Cherry angioma (Campbell de Morgan spot)

A common benign proliferation of small blood vessels forming a bright red, dome-shaped papule, typically on the trunk. Harmless, increasingly common with age, and a straightforward in-clinic vascular-laser target.

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Treatable in-clinic — Vascular laser: KTP 532 nm / Nd:YAG 1064 nm (e.g. Cutera Excel V / V+)

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

Close-up red papules on trunk; de-identified. · Reference image search: Wikimedia · Open-i

Primary causes

Benign vascular (capillary) proliferation — exact trigger unknown.
Age — frequency increases from the 30s onward.
Genetic predisposition.
Reported associations: pregnancy, some chemical exposures (not clinically actionable).

Medications

No pharmacological therapy — cherry angiomas are a vascular-laser / light or electrosurgery target. Removal is cosmetic; confirm the lesion is a typical angioma before treating.

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
KTP 532 nm	Small spot, moderate fluence to blanch the lesion in 1–2 passes.	Superficial bright-red papules; skin types I–IV
Nd:YAG 1064 nm	Higher fluence for larger or deeper/raised lesions.	Larger / thicker angiomas; safer in darker skin

Published ranges are a guide only — confirm against the device manual and supplier protocol, test-spot, and titrate to lesion blanching without epidermal injury. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Electrosurgery / hyfrecation — effective alternative for small lesions.
Reassurance — distinguish from other red papules; benign and does not require removal.

Cautions & contraindications

Confirm the diagnosis — a changing, pigmented or atypical 'red' lesion may not be an angioma; if unsure, refer before treating (amelanotic melanoma can mimic).
Fitzpatrick V–VI / tanned skin — prefer 1064 nm, lower fluence, test spot.
Anticoagulants — counsel on bruising/bleeding.
Post-care — transient crusting/purpura; photoprotection.

Practitioner review — Cherry angioma

B

Recognise & referMalignant · Keratinocytic

Basal cell carcinoma

Basal cell carcinoma (BCC)

The most common skin cancer — a slow-growing, locally invasive tumour that rarely metastasises but destroys local tissue if untreated. Often a pearly papule with telangiectasia, a non-healing sore, or a scaly patch. Recognise and refer.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

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Pearly papule with telangiectasia; non-healing lesion. Use public-domain oncology sources. · Reference image search: Wikimedia · Open-i · NCI Visuals Online

Primary causes

Cumulative and intense UV exposure — the dominant driver.
Fair skin (Fitzpatrick I–II), older age, male sex.
Immunosuppression and prior radiotherapy.
Genetic syndromes (e.g. Gorlin) in a minority.

Recognise & refer

Any pearly, non-healing, bleeding or enlarging lesion — particularly on sun-exposed skin — needs medical assessment and biopsy. Cosmetic treatment must never precede diagnosis.

Medications

Diagnosis and treatment are medical — surgical excision, Mohs, curettage, topical agents (imiquimod, 5-FU) or radiotherapy, directed by a GP/dermatologist. The practitioner role is recognition and referral.

Clinical approach & referral

Recognition and prompt referral — biopsy confirms diagnosis.
Photoprotection counselling and full skin-check advice.
Surveillance — a BCC raises the risk of further skin cancers.

Cautions & contraindications

Never treat a suspicious lesion cosmetically — no peels, laser or resurfacing over a possible BCC.
Non-healing, bleeding or pearly lesions with visible vessels warrant referral.
Document and photograph concerning lesions and direct the patient to a doctor without delay.

Practitioner review — Basal cell carcinoma

B

Aesthetic / dermal-managedVascular · Benign

Broken capillaries

Facial telangiectasia · “broken capillaries”

Small, dilated superficial blood vessels — most often on the nose, cheeks and chin — visible as fine red or purple threads. Benign and very common, frequently overlapping with rosacea and photoageing. A core in-clinic vascular-laser indication.

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Treatable in-clinic — Vascular laser: KTP 532 nm / Nd:YAG 1064 nm (e.g. Cutera Excel V / V+)

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified close-ups of nasal/cheek thread veins; avoid full-face identifiable images. · Reference image search: Wikimedia · Open-i

Primary causes

Chronic UV / photoageing — weakens vessel walls and dermal support.
Rosacea and chronic flushing — neurovascular dilation of facial vessels.
Genetic predisposition / fair skin (Fitzpatrick I–II).
Skin thinning — ageing or topical corticosteroid overuse.
Aggravators: alcohol, heat, temperature extremes, trauma, hormonal factors.

Medications

No specific pharmacological therapy — broken capillaries are a vascular-laser / light indication. Supportive skincare: niacinamide (vitamin B3), azelaic acid where rosacea overlaps, and daily photoprotection to limit recurrence.

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
KTP 532 nm	Spot 1–12 mm · fluence 5–12 J/cm² · pulse 3–15 ms · contact cooling 5–10 °C. Example (fine nasal vessels): 4 mm, 10 J/cm², 15 ms.	Fine, superficial red vessels; skin types I–IV
Nd:YAG 1064 nm	Larger spot, millisecond pulse for deeper/larger or bluish vessels; microsecond mode (e.g. 8 mm, 0.3 ms, 6–7 J/cm²) for diffuse redness.	Deeper / resistant vessels; safer in darker skin

Published starting points for guidance only (Cutera Excel V clinical training; skin types I–IV unless stated). Work from the current device manual, test-spot, and titrate to the clinical endpoint — vessel clearance or spasm without epidermal injury. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

IPL — for diffuse background redness alongside discrete-vessel laser.
Barrier-supportive skincare — niacinamide and azelaic acid where rosacea overlaps.
Photoprotection — mineral SPF to slow recurrence.
Trigger control — manage flushing drivers (heat, alcohol, spicy food).

Cautions & contraindications

Address the underlying driver (rosacea, photoageing) or vessels recur.
Fitzpatrick V–VI and recently tanned skin — higher burn/PIH risk; prefer 1064 nm, lower fluence, mandatory test spot; do not treat tanned skin.
Periorbital treatment — long-pulsed Nd:YAG near the orbit can cause delayed-onset purpura; extreme caution, ocular shields mandatory.
Screen medications — isotretinoin, photosensitisers and anticoagulants affect bruising and healing.
Post-care — photoprotection; avoid heat, exercise and alcohol 24–48 h; counsel on transient purpura.

Practitioner review — Broken capillaries

C

Aesthetic / dermal-managedAcneiform · Pilosebaceous

Comedones

Comedones (blackheads & whiteheads)

Non-inflammatory follicular plugs of keratin and sebum — open (blackheads) or closed (whiteheads). The earliest lesions of acne and a common standalone concern in oily and congested skin.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

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Close-ups of nose/chin open & closed comedones. · Reference image search: Wikimedia · Open-i

Primary causes

Follicular hyperkeratinisation — retained keratinocytes plug the follicle.
Excess sebum — oily skin types.
Comedogenic products / occlusion — heavy cosmetics, certain oils.
Open comedones darken by oxidation, not dirt.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical retinoids (adapalene)	Normalise keratinisation; core comedolytic	TGA
Azelaic acid	Comedolytic, well tolerated	TGA
Salicylic acid (topical)	Keratolytic for congested skin	OTC
Benzoyl peroxide	Prevents progression to inflammatory acne	OTC / TGA

Treatment modalities to investigate

Professional extractions — first-line mechanical clearance with correct technique.
Salicylic / mandelic acid peels — dissolve follicular plugs.
Topical niacinamide — sebum regulation and barrier support.
Non-comedogenic skincare review.

Cautions & contraindications

Avoid traumatic self-extraction — risk of scarring and post-inflammatory pigment.
Retinoid irritation — introduce slowly; daily SPF as retinoids increase photosensitivity.
Darker skin — minimise inflammation to avoid PIH.
Pregnancy — avoid topical retinoids; use azelaic acid.

Practitioner review — Comedones

C

Aesthetic / dermal-managedKnow when to referEczematous · Inflammatory

Contact dermatitis

Contact dermatitis (irritant & allergic)

An eczematous reaction to an external agent — irritant (direct damage) or allergic (delayed hypersensitivity). Red, itchy, sometimes vesicular skin in the pattern of contact. Highly relevant to product and treatment reactions in clinic.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

Localised eczematous reaction in a contact pattern; de-identified. · Reference image search: Wikimedia · Open-i

Primary causes

Irritants — soaps, solvents, acids/retinoids, friction, water exposure.
Allergens — fragrance, preservatives, nickel, rubber, hair dye (PPD), some topical actives.
Impaired barrier increases susceptibility.
Pattern follows the contact area (e.g. earlobes, hands, eyelids).

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical corticosteroids	Mainstay for active flares; potency to site	Script / pharmacy
Emollients	Barrier repair and prevention	OTC
Oral antihistamines	Symptomatic itch relief	OTC
Topical calcineurin inhibitors	Steroid-sparing for face/eyelids	Script

Treatment modalities to investigate

Identify and remove the trigger — the definitive treatment; patch testing for allergic cases (refer).
Barrier repair — bland emollients, gentle cleansing.
Pause active treatments — withhold retinoids/acids/devices until settled.

Cautions & contraindications

Do not perform peels, laser or active treatments on inflamed skin — defer until resolved.
Patch test new actives in reactive patients; document reactions.
Persistent or widespread dermatitis — refer for patch testing / dermatology.
Avoid prolonged potent steroids on the face — risk of atrophy and perioral dermatitis.

Practitioner review — Contact dermatitis

D

Aesthetic / dermal-managedBenign · Keratinocytic

Dermatosis papulosa nigra

Dermatosis papulosa nigra (DPN)

Small, benign, darkly pigmented papules — a variant of seborrhoeic keratosis — typically on the cheeks and periorbital area of darker skin types. Harmless and cosmetic, but requires careful, low-energy technique in pigmented skin.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified periorbital/cheek pigmented papules in darker skin. · Reference image search: Wikimedia · Open-i

Primary causes

Genetic predisposition — strong family history.
Benign keratinocyte proliferation (seborrhoeic keratosis variant).
Common in Fitzpatrick IV–VI; increases with age.
Not caused by sun exposure or poor hygiene.

Medications

No pharmacological treatment — DPN is benign. Removal is cosmetic, by light electrodesiccation, fine-snip/curettage, or carefully-titrated laser; technique must minimise pigment risk.

Treatment modalities to investigate

Light electrodesiccation / hyfrecation — common, effective in trained hands.
Fine curettage / snip excision for raised lesions.
Conservative test patch before treating multiple lesions in darker skin.

Cautions & contraindications

High PIH and hypopigmentation risk in skin of colour — use lowest effective energy, test patch, conservative settings.
Confirm benign diagnosis — if any lesion is atypical, refer.
Counsel on realistic outcomes — temporary darkening is common before fading.
Strict photoprotection post-treatment to limit PIH.

Practitioner review — Dermatosis papulosa nigra

D

Aesthetic / dermal-managedVascular · Inflammatory

Diffuse facial redness

Diffuse facial erythema

Persistent background redness across the central face — distinct from discrete vessels — often the vascular signature of rosacea, photoageing or sensitive/barrier-impaired skin. Responds well to vascular laser and IPL alongside barrier care.

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Treatable in-clinic — Vascular laser: Nd:YAG 1064 nm / KTP 532 nm + IPL (e.g. Cutera Excel V / V+)

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified central-face erythema; avoid identifiable images. · Reference image search: Wikimedia · Open-i

Primary causes

Rosacea (erythematotelangiectatic) — neurovascular dysregulation.
Photoageing — chronic UV vascular and dermal change.
Barrier impairment / sensitive skin — over-exfoliation, harsh actives.
Aggravators: heat, alcohol, spicy food, temperature extremes, stress.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Brimonidine 0.5% (Mirvaso)	Temporary vasoconstriction for erythema	Script
Topical ivermectin / metronidazole / azelaic acid	Where rosacea drives the redness	Script / TGA

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
Nd:YAG 1064 nm (microsecond)	e.g. 8 mm spot, ~0.3 ms, 6–7 J/cm² for diffuse redness; multiple gentle passes.	Background erythema; safer in darker skin
KTP 532 nm / IPL	For superimposed fine vessels and background tone.	Adjunct to discrete-vessel work

Guidance only — confirm against the device manual and supplier protocol, test-spot, and titrate to gentle erythema/endpoint without epidermal injury. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Barrier-repair skincare — niacinamide, ceramides; stop harsh actives.
IPL for diffuse redness and tone.
Trigger identification and photoprotection (mineral SPF).
LED red/near-infrared for anti-inflammatory support.

Cautions & contraindications

Brimonidine rebound — redness can worsen as it wears off; trial cautiously.
Treat the driver (rosacea, barrier) or redness returns.
Avoid heat-based facials and aggressive exfoliation on reactive skin.
Fitzpatrick V–VI / tanned skin — prefer 1064 nm, lower fluence, test spot.

Practitioner review — Diffuse facial redness

E

Aesthetic / dermal-managedKnow when to referEczematous · Chronic

Eczema (atopic dermatitis)

Atopic dermatitis

A chronic, relapsing, itchy inflammatory skin disease with a defective barrier and immune dysregulation. Flexural in distribution, often atopic. Managed conservatively in aesthetics — control the barrier, avoid triggering procedures, refer when severe.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

Flexural eczematous changes; de-identified. · Reference image search: Wikimedia · Open-i

Primary causes

Skin-barrier dysfunction — filaggrin and lipid abnormalities.
Immune dysregulation — Th2-skewed inflammation.
Genetic / atopic predisposition (asthma, hay fever).
Triggers: irritants, allergens, heat, sweat, stress, infection.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Emollients	Foundation of care — barrier repair	OTC
Topical corticosteroids	Flare control; potency to site/severity	Script / pharmacy
Topical calcineurin inhibitors	Steroid-sparing, face/folds	Script
Systemic / biologics (e.g. dupilumab)	Moderate–severe; specialist	Specialist

Treatment modalities to investigate

Barrier-first skincare — bland emollients, gentle non-foaming cleansers.
Trigger avoidance — fragrance, harsh actives, overheating.
Defer elective procedures until skin is settled.

Cautions & contraindications

Do not peel, laser or use strong actives on active eczema — high irritation and flare risk.
Eczema herpeticum (painful clustered vesicles, unwell) — urgent medical referral.
Secondary infection (weeping, crusting) — medical review.
Severe/refractory disease — refer to dermatology.

Practitioner review — Eczema (atopic dermatitis)

E

Aesthetic / dermal-managedPigmentary · Benign

Ephelides (freckles)

Small, well-defined tan-brown macules that darken with sun exposure and fade in winter, common in fair skin. Benign; a cosmetic pigment concern that responds to photoprotection and pigment-directed light/laser.

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Treatable in-clinic — Pigment-capable laser / IPL: KTP 532 nm (e.g. Cutera Excel V / V+)

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified cheek/nose freckling in fair skin. · Reference image search: Wikimedia · Open-i

Primary causes

Genetic predisposition (fair skin, MC1R variants).
UV exposure — stimulates focal melanin without increasing melanocyte number.
Darken in summer, fade in winter.
Distinct from solar lentigines (which are persistent).

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical brighteners	Niacinamide, vitamin C, azelaic acid — adjuncts	Cosmeceutical

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
KTP 532 nm / IPL	Pigment-selective settings to lighten focal macules.	Fair skin (I–III); avoid in tanned skin

Guidance only — confirm device settings and suitability; freckles recur without photoprotection. Test-spot pigmented lesions and rule out atypia first. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Daily broad-spectrum SPF — primary management; prevents darkening and recurrence.
Topical antioxidants / brighteners as adjuncts.
Gentle pigment peels in suitable skin types.

Cautions & contraindications

Distinguish from lentigo maligna / atypical pigment — if a 'freckle' is changing, asymmetric or irregular, refer before any treatment.
Avoid treating tanned skin — burn and PIH risk.
Recurrence is expected without strict photoprotection.
Darker skin types — high PIH risk with pigment devices; conservative approach.

Practitioner review — Ephelides (freckles)

F

Aesthetic / dermal-managedKnow when to referInflammatory · Infective

Folliculitis

Inflammation of hair follicles producing small, sometimes itchy or tender pustules and papules around follicular openings. Usually superficial; causes range from bacterial to fungal, mechanical and post-procedure.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

Follicular pustules/papules; de-identified. · Reference image search: Wikimedia · Open-i

Primary causes

Bacterial — commonly Staphylococcus aureus.
Malassezia (fungal) folliculitis — itchy, monomorphic, trunk/upper back.
Mechanical / occlusive — shaving, friction, heavy products, sweat.
Pseudomonas ('hot tub') — after contaminated water exposure.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical antiseptics / antibiotics	Mild bacterial cases	Pharmacy / Script
Oral antibiotics	Extensive or recurrent bacterial folliculitis	Script
Topical/oral antifungals	Malassezia folliculitis (won't respond to antibiotics)	Pharmacy / Script

Treatment modalities to investigate

Identify the cause — bacterial vs fungal changes treatment entirely.
Reduce mechanical triggers — shaving technique, breathable clothing, fewer occlusive products.
Antiseptic washes as adjunct/prevention.

Cautions & contraindications

Do not treat over active folliculitis — defer peels/laser/waxing until cleared.
Malassezia folliculitis is misdiagnosed as acne — antibiotics worsen it; suspect if itchy and monomorphic.
Fever, spreading redness or systemic illness — medical referral (possible furuncle/cellulitis).
Recurrent / treatment-resistant cases — refer for swab and review.

Practitioner review — Folliculitis

H

Aesthetic / dermal-managedKnow when to referVascular · Benign

Haemangioma

A benign proliferation of blood vessels. Infantile haemangiomas appear and grow in babies and are a paediatric matter; adult cherry/lobular forms are common and benign. Some respond to vascular laser; growth or atypical features need medical assessment.

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Treatable in-clinic — Vascular laser: KTP 532 nm / Nd:YAG 1064 nm (e.g. Cutera Excel V / V+)

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified benign vascular papule examples. · Reference image search: Wikimedia · Open-i

Primary causes

Benign vascular proliferation — endothelial overgrowth.
Infantile type — appears in early infancy, proliferates then involutes.
Adult cherry/lobular forms — increase with age.
Most are idiopathic; not caused by injury or diet.

Medications

Adult superficial lesions can be treated with vascular laser; infantile haemangiomas are managed medically (observation or oral propranolol) by paediatrics/dermatology — refer.

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
KTP 532 nm	Superficial lesions; moderate fluence to blanch.	Small superficial adult lesions; I–IV
Nd:YAG 1064 nm	Higher fluence for thicker/deeper lesions.	Larger/raised lesions; darker skin

Guidance only — confirm device protocol, test-spot, titrate to blanching. Refer any rapidly growing, ulcerating or infantile lesion before treating. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Diagnosis first — confirm benign before cosmetic laser.
Refer infantile haemangiomas to paediatrics/dermatology.
Reassurance for typical benign adult lesions.

Cautions & contraindications

Infantile, periocular, airway or rapidly growing lesions — refer urgently; do not treat cosmetically.
Ulceration or bleeding — medical review.
Fitzpatrick V–VI / tanned skin — prefer 1064 nm, lower fluence, test spot.
Atypical vascular lesions — exclude vascular malformation/malignancy by referral.

Practitioner review — Haemangioma

H

Aesthetic / dermal-managedKnow when to referInfective · Viral

Herpes simplex (cold sores)

Herpes simplex virus (HSV) — orolabial

A recurrent viral infection causing grouped vesicles on an erythematous base, typically at the lip border, often with a prodromal tingle. Critically relevant to aesthetics: procedures can trigger reactivation, and active lesions are a contraindication.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified grouped perioral vesicles. · Reference image search: Wikimedia · Open-i

Primary causes

HSV-1 (usually) reactivation from the trigeminal ganglion.
Triggers — UV, fever, stress, trauma, and skin procedures (peels, laser, microneedling, dermal filler).
Prodrome — tingling/burning before vesicles.
Contagious when active.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Aciclovir / valaciclovir / famciclovir	Antivirals — treat and prevent reactivation	Script / pharmacy
Topical antivirals	Mild orolabial episodes	Pharmacy

Treatment modalities to investigate

Antiviral prophylaxis for patients with a cold-sore history before resurfacing, laser, microneedling or perioral filler.
Reschedule procedures if a lesion is active.
Photoprotection to reduce UV-triggered recurrences.

Cautions & contraindications

Active herpes is a contraindication to facial procedures — defer until healed; treating through it risks dissemination and scarring.
Always screen for cold-sore history before perioral procedures and prescribe prophylaxis where indicated.
Eczema herpeticum (widespread, unwell) — urgent medical referral.
Avoid cross-contamination — strict infection control with active lesions.

Practitioner review — Herpes simplex (cold sores)

H

Recognise & referInflammatory · Chronic

Hidradenitis suppurativa

A chronic, painful, scarring inflammatory disease of apocrine-bearing skin (axillae, groin, under breasts) with recurrent nodules, abscesses, sinus tracts and scarring. Frequently under-recognised; needs medical management, not cosmetic treatment.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified axillary/groin lesions; sensitive — prefer clinical-diagram or de-identified sources. · Reference image search: Wikimedia · Open-i

Primary causes

Follicular occlusion and rupture with secondary inflammation.
Genetic predisposition; strong familial pattern.
Risk factors — smoking, obesity, friction, hormonal factors.
Not an infection or hygiene problem (though secondary infection occurs).

Recognise & refer

Recurrent painful nodules, abscesses or sinus tracts in the axillae, groin or under the breasts indicate hidradenitis suppurativa — refer for medical diagnosis and staged treatment rather than cosmetic intervention.

Clinically proven treatments (medically directed)

Agent	Class / clinical use	Status
Topical/oral antibiotics	Anti-inflammatory and antimicrobial role	Script
Hormonal therapy	Selected patients	Script
Biologics (e.g. adalimumab)	Moderate–severe; specialist	Specialist
Surgery	Deroofing/excision of tracts	Specialist

Clinical approach & referral

Early recognition and referral to dermatology — disease is staged (Hurley).
Lifestyle support — smoking cessation, weight, friction reduction.
Laser hair reduction (Nd:YAG) is an adjunct in selected cases, specialist-guided.

Cautions & contraindications

Do not treat active lesions cosmetically — refer for diagnosis and staging.
Often misdiagnosed as recurrent boils/acne — recognise the apocrine pattern and scarring.
Significant pain and psychosocial burden — manage with empathy and prompt referral.
Secondary infection / systemic symptoms — medical review.

Practitioner review — Hidradenitis suppurativa

H

Aesthetic / dermal-managedPigmentary

Hyperpigmentation (PIH)

Post-inflammatory hyperpigmentation & general dyschromia

Excess melanin deposition following inflammation or injury — flat brown to grey-brown patches at sites of prior acne, dermatitis, or procedures. Especially common and persistent in darker skin; prevention and gentle, gradual correction are key.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified PIH macules at prior acne sites in skin of colour. · Reference image search: Wikimedia · Open-i

Primary causes

Prior inflammation/injury — acne, dermatitis, burns, over-aggressive procedures.
UV exposure — deepens and prolongs pigment.
Darker skin types (Fitzpatrick III–VI) — greater melanocyte reactivity.
Distinct from melasma (which is hormonally driven and relapsing).

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Azelaic acid	Tyrosinase inhibitor; pregnancy-safe	TGA
Hydroquinone	Depigmenting; time-limited courses	Script / compounded
Topical retinoids	Accelerate pigment turnover	TGA / Script

Treatment modalities to investigate

Photoprotection first — SPF 50+ (iron oxides for visible light) underpins everything.
Topical brighteners — niacinamide (vitamin B3), vitamin C, azelaic acid, kojic acid.
Gentle chemical peels — mandelic/lactic; conservative in darker skin.
Treat the underlying cause (e.g. control acne) to stop new pigment.

Cautions & contraindications

Aggressive lasers/peels can worsen PIH — especially in darker skin; conservative settings, test patches.
Avoid treating tanned skin; reinforce photoprotection.
Set expectations — fading is gradual (months).
Exclude other pigment causes (melasma, drug-induced, atypical lesions) before treating.

Practitioner review — Hyperpigmentation (PIH)

I

Aesthetic / dermal-managedInflammatory · Hair

Ingrown hairs (PFB)

Pseudofolliculitis barbae / ingrown hairs

Inflammatory papules and pustules caused by hairs re-entering the skin after shaving, common in the beard area and in coarse or curly hair. Can lead to post-inflammatory pigment and scarring; laser hair reduction is often definitive.

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Treatable in-clinic — Hair-reduction laser: Nd:YAG 1064 nm (e.g. Cutera Excel V / V+ Nd:YAG, or dedicated hair laser)

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified beard-area papules/ingrown hairs. · Reference image search: Wikimedia · Open-i

Primary causes

Curved/curly hair re-entering the skin after close shaving.
Close shaving / plucking sharpening the hair tip.
Coarse hair and darker skin — higher susceptibility.
Secondary inflammation and PIH/keloidal scarring can follow.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical retinoids	Reduce hyperkeratosis around follicle	TGA / Script
Topical/oral antibiotics	If secondary infection	Script
Mild topical steroid (short)	Settle inflammation	Pharmacy / Script

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
Nd:YAG 1064 nm	Hair-reduction settings; safest wavelength for darker skin.	Definitive option; reduces hair density and recurrence

Guidance only — confirm device hair-reduction protocol and suitability; Nd:YAG preferred in darker skin. Test-spot and titrate. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Laser hair reduction (Nd:YAG) — often the definitive solution.
Shaving technique — single-blade, with grain, no stretching; or grow the beard.
Gentle exfoliation to free trapped hairs.
Manage PIH with photoprotection and brighteners.

Cautions & contraindications

Darker skin — Nd:YAG preferred; conservative settings to avoid burns/PIH.
Do not treat actively infected/inflamed areas until settled.
Keloidal folliculitis (nape) — refer if scarring/keloid forms.
Avoid plucking/waxing which can worsen the cycle.

Practitioner review — Ingrown hairs (PFB)

K

Aesthetic / dermal-managedKnow when to referScarring · Fibroproliferative

Keloid & hypertrophic scars

Keloid and hypertrophic scarring

Raised scars from excess collagen during healing. Hypertrophic scars stay within the wound; keloids extend beyond it and can grow over time. Treatment is multimodal and prone to recurrence — and certain procedures can provoke them.

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Treatable in-clinic — Vascular laser adjunct: Nd:YAG / PDL for redness & pliability (e.g. Cutera Excel V / V+)

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified raised scars (earlobe/chest). · Reference image search: Wikimedia · Open-i

Primary causes

Excess collagen deposition during wound healing.
Genetic predisposition and darker skin types (keloids).
Wound tension / site — chest, shoulders, earlobes.
Triggers — surgery, piercings, acne, burns, and some skin procedures.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Intralesional corticosteroids	First-line to flatten/soften	Script / medical
Silicone gel/sheeting	Evidence-based scar management	OTC
Intralesional 5-FU	Adjunct in resistant keloids	Specialist

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
Vascular laser (PDL / Nd:YAG)	Reduce erythema and improve pliability; series of sessions.	Adjunct, often with steroid injection

Guidance only — keloid treatment is multimodal and specialist-led; confirm protocol. Avoid provoking new keloids in predisposed patients. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Silicone + pressure — first-line conservative management.
Intralesional steroid ± laser combinations.
Avoid elective procedures that risk new keloids in predisposed patients.
Refer established/growing keloids for specialist combination therapy.

Cautions & contraindications

Screen for keloid tendency before elective procedures (microneedling, piercings, ablative laser, surgery).
Recurrence is common — counsel and use combination approaches.
Surgical excision alone often worsens keloids — only with adjuvant therapy.
Darker skin — higher keloid risk; conservative approach.

Practitioner review — Keloid & hypertrophic scars

K

Aesthetic / dermal-managedKeratinisation · Benign

Keratosis pilaris

A very common, benign condition of rough, small follicular bumps — 'chicken skin' — usually on the upper arms, thighs and cheeks, sometimes with background redness. Harmless and cosmetic; managed with keratolytics and gentle exfoliation.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified upper-arm/cheek follicular bumps. · Reference image search: Wikimedia · Open-i

Primary causes

Follicular hyperkeratinisation — keratin plugs at follicle openings.
Genetic predisposition; often improves with age.
Association with dry skin / atopy.
Worse in dry/winter conditions.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Keratolytics (urea, lactic, salicylic acid)	Smooth follicular plugging	OTC / pharmacy
Topical retinoids	Normalise keratinisation in resistant cases	TGA / Script

Treatment modalities to investigate

Emollients + keratolytics — mainstay (urea, AHAs).
Gentle exfoliation — avoid aggressive scrubbing.
Vascular laser / IPL for persistent background redness (KP rubra).
Realistic expectations — texture improves; condition is chronic.

Cautions & contraindications

Avoid harsh physical scrubs — worsen irritation and redness.
Do not over-treat — benign and often self-limiting.
Darker skin — minimise inflammation to avoid PIH.
Distinguish from acne/folliculitis to avoid mistreatment.

Practitioner review — Keratosis pilaris

L

Recognise & referAutoimmune · Inflammatory

Cutaneous lupus

Cutaneous lupus erythematosus

An autoimmune condition with photosensitive facial rashes — including the malar 'butterfly' rash and scarring discoid plaques. Easily mistaken for rosacea or pigmentation; misdiagnosis delays care, so recognise and refer.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified malar/discoid lesions; prefer clinical-reference sources. · Reference image search: Wikimedia · Open-i

Primary causes

Autoimmune inflammation targeting skin (± systemic involvement).
UV exposure — strong photosensitivity trigger.
Genetic and hormonal factors.
Some drug-induced forms.

Recognise & refer

A persistent photosensitive malar rash or scarring discoid plaques may be cutaneous lupus, not rosacea or pigmentation. Refer for diagnosis and a systemic screen before any cosmetic treatment.

Clinically proven treatments (medically directed)

Agent	Class / clinical use	Status
Topical/intralesional steroids	Active cutaneous lesions; medical	Script
Antimalarials (hydroxychloroquine)	Mainstay systemic therapy	Specialist
Photoprotection	Essential adjunct	OTC

Clinical approach & referral

Recognition and referral — rheumatology/dermatology for diagnosis and systemic screen.
Strict photoprotection counselling.
Avoid cosmetic procedures on active disease.

Cautions & contraindications

Do not treat as rosacea/pigmentation — a fixed photosensitive malar rash or scarring discoid plaques need medical assessment.
Procedures and UV can flare disease — defer and refer.
Scarring/atrophy from discoid lupus — early referral matters.
Screen for systemic symptoms (joints, fatigue) and refer.

Practitioner review — Cutaneous lupus

L

Aesthetic / dermal-managedKnow when to referVascular · Benign

Leg veins (spider & reticular)

Lower-limb telangiectasia & reticular veins

Superficial spider (red) and reticular (blue-green) veins of the legs — cosmetic, but sometimes the visible sign of underlying venous insufficiency. Screen the venous system first; suitable vessels respond to Nd:YAG laser or sclerotherapy.

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Treatable in-clinic — Vascular laser: Nd:YAG 1064 nm (e.g. Cutera Excel V / V+); sclerotherapy alternative

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified lower-limb spider/reticular veins. · Reference image search: Wikimedia · Open-i

Primary causes

Venous hypertension / valve incompetence — often underlying.
Genetic predisposition, female sex, pregnancy, prolonged standing.
Hormonal factors and age.
Reticular veins frequently feed spider veins.

Medications

Not a pharmacological condition. Treated by Nd:YAG laser or sclerotherapy after venous assessment. Larger/feeding veins must be addressed or surface treatment fails and recurs.

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
Nd:YAG 1064 nm	Long-pulsed, higher fluence for leg telangiectasia; spot/fluence to vessel calibre.	Fine–medium leg vessels; deeper penetration

Guidance only — confirm device leg-vein protocol, test-spot, titrate to vessel spasm/clearance. Rule out venous insufficiency before treating. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Venous assessment first — exclude/treat reflux (refer for duplex if signs of insufficiency).
Sclerotherapy — often first-line for many leg vessels.
Nd:YAG laser for needle-phobic patients or vessels unsuitable for sclerotherapy.
Compression post-treatment as indicated.

Cautions & contraindications

Screen for venous insufficiency — varicosities, aching, swelling, skin changes warrant referral before cosmetic treatment.
Leg vessels carry higher risk of PIH, matting and pigmentation — counsel and conservative settings.
Avoid in pregnancy and screen for clotting risk.
Darker skin — Nd:YAG with care; test spot.

Practitioner review — Leg veins (spider & reticular)

L

Aesthetic / dermal-managedPigmentary · Photoageing

Solar lentigines

Solar lentigines (sun spots / age spots)

Persistent, well-defined brown macules on chronically sun-exposed skin (face, hands, décolletage) — a hallmark of photoageing. Benign, but must be distinguished from lentigo maligna. Respond well to pigment-directed laser, IPL and topicals.

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Treatable in-clinic — Pigment-capable laser / IPL: KTP 532 nm (e.g. Cutera Excel V / V+)

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified facial/hand lentigines; exclude atypical lesions. · Reference image search: Wikimedia · Open-i

Primary causes

Cumulative UV exposure — increased melanin and melanocyte activity.
Photoageing — sun-exposed sites.
Fair skin and increasing age.
Persistent (unlike freckles), do not fade in winter.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical brighteners	Niacinamide, vitamin C, azelaic acid, retinoids	Cosmeceutical / Script
Hydroquinone	Targeted lightening, time-limited	Script / compounded

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
KTP 532 nm / IPL	Pigment-selective settings to lift discrete lentigines.	Lighter skin; avoid in tanned skin

Guidance only — confirm settings/suitability, test-spot. Always exclude lentigo maligna before treating a pigmented facial macule. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Pigment laser / IPL — effective for discrete lesions.
Daily photoprotection — prevents new lesions and recurrence.
Topical brighteners and gentle peels as adjuncts.
Dermoscopy / assessment of any atypical lesion first.

Cautions & contraindications

Exclude lentigo maligna (melanoma in situ) — any asymmetric, irregular, changing or variably pigmented facial macule must be assessed/referred before laser.
Avoid treating tanned skin — burn/PIH risk.
Darker skin — high PIH risk with pigment devices; conservative.
Recurrence without photoprotection.

Practitioner review — Solar lentigines

M

Recognise & referMalignant · Melanocytic

Melanoma

The most dangerous skin cancer — a malignancy of melanocytes that can metastasise. Early recognition saves lives. Australia has among the world's highest rates. Any suspicious pigmented or changing lesion is an urgent referral, never a cosmetic target.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

ABCDE examples; use public-domain oncology sources. · Reference image search: Wikimedia · Open-i · NCI Visuals Online

Primary causes

UV exposure — intense/intermittent and cumulative; sunburns.
Many or atypical naevi, fair skin, family/personal history.
Genetic factors and immunosuppression.
Can arise de novo or within an existing mole.

Recognise & refer

Any new, changing, asymmetric, multi-coloured, enlarging or bleeding pigmented lesion — or an 'ugly duckling' that stands out — requires urgent medical assessment. Cosmetic treatment is absolutely contraindicated until melanoma is excluded.

Medications

Diagnosis is by urgent excision biopsy and histology; treatment (surgery ± systemic therapy) is specialist-led. The practitioner role is recognition and urgent referral.

Clinical approach & referral

Apply ABCDE / 'ugly duckling' — Asymmetry, Border, Colour, Diameter, Evolving.
Urgent referral of any suspicious lesion to a GP/skin-cancer clinic/dermatologist.
Photoprotection and skin-check advocacy with every patient.

Cautions & contraindications

Never laser, peel, treat or remove a suspicious pigmented lesion — this destroys diagnostic tissue and can be catastrophic.
A changing, new, irregular or bleeding pigmented lesion is urgent — refer immediately.
Amelanotic melanoma can be pink/red and mimic benign lesions — maintain suspicion.
Document and direct to a doctor; do not reassure or delay.

Practitioner review — Melanoma

M

Aesthetic / dermal-managedPigmentary · Chronic / relapsing

Melasma

Melasma (chloasma)

An acquired, symmetrical hyperpigmentation of sun-exposed skin — cheeks, forehead, upper lip, jawline. Chronic and relapsing, with a strong tendency to rebound after over-aggressive treatment. Demands a conservative, photoprotection-led approach.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

Centrofacial pattern + (if possible) Wood's-lamp depth and a darker-phototype case. · Reference image search: Wikimedia · Open-i

Primary causes

UV and visible light — the dominant driver; visible/blue light significant in darker skin.
Hormonal influence — pregnancy, the COCP, hormonal therapy.
Genetic predisposition and Fitzpatrick III–VI.
Heat — infrared/thermal stimulation aggravates.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Hydroquinone 2–4%	Tyrosinase inhibitor; first-line, time-limited	Script / compounded
Triple combination (Kligman's)	HQ + tretinoin + fluocinolone — gold standard	Compounded
Azelaic acid 15–20%	Pregnancy-safe alternative	TGA
Tranexamic acid	Oral (off-label) / topical; prescriber-screened	Script (off-label)

Treatment modalities to investigate

Photoprotection first — always — SPF 50+ with iron oxides for visible light.
Topical niacinamide (vitamin B3) — inhibits melanosome transfer.
Gentle peels (mandelic/lactic/azelaic) — conservative in darker skin.
Low-fluence Q-switched Nd:YAG ('toning') — experienced hands only, with adjuncts.

Cautions & contraindications

IPL and ablative/high-energy lasers can severely worsen melasma and trigger PIH — heat is a trigger; avoid aggressive devices.
Darker phototypes (IV–VI) — highest rebound/PIH risk; conservative settings.
Prolonged high-strength hydroquinone — ochronosis risk; cycle courses.
Oral tranexamic acid contraindicated with thromboembolic risk — screen.
Set expectations — controlled, not cured; over-treatment deteriorates it.

Practitioner review — Melasma

M

Aesthetic / dermal-managedCystic · Benign

Milia

Tiny, firm, white keratin-filled cysts just beneath the skin surface — common around the eyes and cheeks. Benign and harmless; readily removed in clinic with simple technique.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified periocular white papules. · Reference image search: Wikimedia · Open-i

Primary causes

Trapped keratin in a follicle or sweat duct.
Primary (spontaneous) or secondary (after trauma, burns, blistering, occlusive products).
Common in newborns and adults alike.
Not related to diet or hygiene.

Medications

No medication required — milia are removed by simple extraction (lance and express) with sterile technique. Topical retinoids may help recurrence-prone skin.

Treatment modalities to investigate

Manual de-roofing and extraction — sterile lance/needle and comedone extractor.
Topical retinoids for prevention in prone patients.
Review occlusive products that may contribute.

Cautions & contraindications

Sterile technique to avoid infection/scarring, especially near the eyes.
Periorbital caution — gentle, precise technique.
Confirm diagnosis — distinguish from syringoma/other papules.
Avoid aggressive treatment — benign and superficial.

Practitioner review — Milia

M

Aesthetic / dermal-managedKnow when to referInfective · Viral

Molluscum contagiosum

A common viral infection causing small, firm, dome-shaped papules with a central dimple (umbilication). Self-limiting but contagious and spreadable by scratching or shaving. Recognise to avoid spreading it during treatments.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified umbilicated papules. · Reference image search: Wikimedia · Open-i

Primary causes

Poxvirus (molluscum contagiosum virus) — skin-to-skin or fomite spread.
Autoinoculation — scratching, shaving, waxing spread lesions.
More extensive in atopic or immunosuppressed patients.
Common in children; genital lesions in adults may be sexually transmitted.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Observation	Often self-resolves over months	—
Cryotherapy / curettage	Physical removal	Medical
Topical agents	e.g. podophyllotoxin/cantharidin in selected cases	Script / medical

Treatment modalities to investigate

Recognition — avoid shaving/waxing/treating over lesions (spreads them).
Conservative approach — many resolve without treatment.
Refer widespread, genital, or immunosuppressed cases.

Cautions & contraindications

Do not wax, shave or perform procedures over lesions — high autoinoculation risk.
Infection control — contagious; avoid cross-contamination.
Genital lesions in adults — refer for STI assessment.
Extensive/atypical disease — consider immunosuppression; refer.

Practitioner review — Molluscum contagiosum

N

Recognise & referMelanocytic · Benign

Naevi (moles)

Melanocytic naevi (moles)

Benign clusters of melanocytes — common, and usually harmless. The clinical priority is distinguishing benign moles from atypical lesions and melanoma. Moles are assessed and (if needed) removed medically, never lasered cosmetically.

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Clinical example

De-identified, licence-cleared

⛳

Close-up / detail

Add from sources at right

Benign vs atypical naevi for contrast; de-identified / public-domain. · Reference image search: Wikimedia · Open-i

Primary causes

Benign melanocyte proliferation — congenital or acquired.
Genetic factors and UV exposure influence number.
Atypical (dysplastic) naevi carry higher melanoma risk.
Changes at puberty and pregnancy can occur.

Recognise & refer

Moles should be assessed medically — any that need removal are excised with histology, never lasered. Refer changing or atypical lesions for melanoma exclusion.

Medications

Moles are not a cosmetic-laser target. Any mole needing removal should be assessed and excised medically so histology can be performed. The practitioner role is recognition and referral of atypical lesions.

Clinical approach & referral

Monitor with ABCDE / 'ugly duckling' and refer changes.
Medical excision with histology for any lesion requiring removal.
Photoprotection and skin-check advocacy.

Cautions & contraindications

Never laser or shave off a mole cosmetically — this destroys diagnostic tissue and can mask melanoma.
Refer any changing, atypical, symptomatic or new pigmented lesion.
Document and photograph lesions of concern.
Do not reassure an atypical lesion — direct to medical assessment.

Practitioner review — Naevi (moles)

P

Aesthetic / dermal-managedKnow when to referInflammatory · Acneiform

Perioral dermatitis

A facial eruption of small papules and pustules around the mouth (sparing the lip border), sometimes the nose and eyes, with mild scaling. Often triggered by topical corticosteroids — which paradoxically must be stopped, not continued.

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Clinical example

De-identified, licence-cleared

⛳

Close-up / detail

Add from sources at right

De-identified perioral papulopustular eruption sparing lip margin. · Reference image search: Wikimedia · Open-i

Primary causes

Topical corticosteroid use on the face — a key trigger.
Occlusive cosmetics/heavy moisturisers and fluoride toothpaste in some.
Skin-barrier and microbiome disturbance.
Predominantly affects women 20–45.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical metronidazole / azelaic acid / ivermectin	First-line anti-inflammatory topicals	Script / TGA
Oral tetracyclines (doxycycline)	Moderate/resistant cases	Script
'Zero-therapy'	Stop all topical steroids and heavy products	—

Treatment modalities to investigate

Stop topical corticosteroids — central to recovery (expect a transient flare).
Simplify skincare — gentle cleanser, minimal products, no occlusives.
Avoid actives and procedures until settled.

Cautions & contraindications

Do not treat with topical steroids — they cause/perpetuate it; counsel patients on the temporary rebound when stopping.
Defer peels/laser/actives on active disease.
Distinguish from acne/rosacea to avoid mistreatment.
Refer persistent or diagnostically unclear cases.

Practitioner review — Perioral dermatitis

P

Aesthetic / dermal-managedVascular · Benign

Periorbital veins

Periorbital (infraorbital) reticular veins

Prominent blue-green reticular veins around and below the eyes that can create a tired or shadowed appearance. Treatable with long-pulsed Nd:YAG — but the periorbital location demands the highest caution and mandatory eye protection.

⚡

Treatable in-clinic — Vascular laser: Nd:YAG 1064 nm (e.g. Cutera Excel V / V+) — periorbital, high caution

⛳

Clinical example

De-identified, licence-cleared

⛳

Close-up / detail

Add from sources at right

De-identified infraorbital reticular veins. · Reference image search: Wikimedia · Open-i

Primary causes

Thin periorbital skin revealing underlying reticular veins.
Genetic predisposition and ageing (fat/volume loss).
Sun exposure contributing to skin thinning.
More visible with fair, thin skin.

Medications

No pharmacological treatment — prominent periorbital veins are treated with long-pulsed Nd:YAG laser by experienced practitioners with full ocular protection.

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
Nd:YAG 1064 nm	Long-pulsed, larger spot; higher fluence/longer pulse for these calibre vessels (e.g. published case use ~4 mm, ~25 ms, high fluence).	Reticular periorbital veins; experienced operators only

Guidance only — periorbital Nd:YAG can cause delayed-onset purpura; confirm device protocol, use corneal/scleral eye shields, test-spot and titrate conservatively. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Long-pulsed Nd:YAG — the principal modality.
Meticulous eye protection — internal ocular shields mandatory.
Conservative, staged sessions to limit bruising.

Cautions & contraindications

Mandatory ocular shields — never treat near the eye without proper corneal/scleral protection.
Delayed-onset purpura is recognised after periorbital Nd:YAG — counsel and treat conservatively.
Experienced operators only — high-risk site.
Screen anticoagulants/photosensitisers and set realistic expectations.

Practitioner review — Periorbital veins

P

Aesthetic / dermal-managedAgeing · UV-induced

Photoageing

Photoageing (dermatoheliosis)

The cumulative skin changes of chronic UV exposure — fine lines, coarse wrinkles, dyspigmentation, telangiectasia, sallowness and loss of elasticity. The core canvas of aesthetic practice, with a deep toolkit and a foundation of photoprotection.

⚡

Treatable in-clinic — Resurfacing & pigment/vascular devices (laser, IPL, RF) — device-dependent

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified photoaged skin (dyspigmentation, wrinkling). · Reference image search: Wikimedia · Open-i

Primary causes

Chronic UV exposure — collagen/elastin degradation, dyspigmentation, vascular change.
Visible light and infrared contributions.
Smoking and pollution accelerate it.
Superimposed on intrinsic (chronological) ageing.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical retinoids	Best-evidenced topical for photoageing	TGA / Script
Antioxidants (vitamin C)	Adjunct photoprotection/repair	Cosmeceutical

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
Resurfacing lasers (non-ablative / ablative fractional)	Texture, lines, tone — device- and skin-type-dependent.	Stronger results, more downtime/risk
IPL / pigment & vascular laser	Lentigines, redness, telangiectasia.	Tone and vascular components

Guidance only — modality and parameters are device- and Fitzpatrick-dependent; confirm protocols, test-spot, and manage darker-skin risk conservatively. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Daily broad-spectrum SPF — the foundation; prevents further damage.
Topical retinoids and antioxidants.
Resurfacing — peels, microneedling, fractional laser, RF.
Pigment/vascular devices for lentigines and redness.

Cautions & contraindications

Exclude skin cancer first — photoaged skin is high-risk; assess suspicious lesions before resurfacing.
Darker skin — PIH risk; conservative settings, test patches.
Retinoids — photosensitivity and pregnancy contraindication.
Match modality to downtime/expectations and avoid over-treatment.

Practitioner review — Photoageing

P

Aesthetic / dermal-managedVascular · Pigmentary · Photoageing

Poikiloderma of Civatte

Chronic sun-induced change of the neck and upper chest combining redness, telangiectasia and brown pigmentation, characteristically sparing the shaded submental area. A classic photoageing pattern that responds to IPL and vascular/pigment laser.

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Treatable in-clinic — Vascular + pigment laser / IPL: KTP 532 nm + Nd:YAG 1064 nm (e.g. Cutera Excel V / V+)

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified neck/décolletage redness + pigment sparing submental area. · Reference image search: Wikimedia · Open-i

Primary causes

Chronic cumulative UV exposure of the neck/décolletage.
Fair skin and photoageing.
Possible photosensitising cosmetic component (historically).
Spares the sun-protected submental shadow.

Medications

No pharmacological cure — treated with IPL and vascular/pigment laser plus strict photoprotection. The neck is a cautious area for energy devices.

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
IPL	Workhorse for combined redness + pigment on the décolletage.	Lighter skin; conservative on the neck
KTP 532 / Nd:YAG 1064 nm	Discrete vessels and pigment; gentle settings.	Targeted vascular/pigment component

Guidance only — neck skin heals less robustly than the face; use conservative settings, test-spot, and titrate carefully. Confirm device protocol. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

IPL — first-line for the mixed presentation.
Vascular/pigment laser for residual vessels and lentigines.
Strict daily photoprotection — essential to prevent progression/recurrence.
Topical antioxidants/retinoids as adjuncts.

Cautions & contraindications

The neck is higher-risk for scarring and pigment change — conservative settings, test patches, avoid aggressive fluences.
Avoid treating tanned skin; reinforce photoprotection.
Darker skin — significant PIH risk; cautious approach.
Realistic expectations — staged improvement, maintenance needed.

Practitioner review — Poikiloderma of Civatte

P

Aesthetic / dermal-managedKnow when to referVascular · Congenital

Port wine stain

Port wine stain (capillary malformation)

A congenital capillary malformation present from birth — a flat red-purple patch, often facial, that persists and can darken and thicken with age. Treatable with vascular laser; some carry syndromic associations requiring medical work-up.

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Treatable in-clinic — Vascular laser: KTP 532 nm / Nd:YAG 1064 nm; PDL is gold standard (e.g. Cutera Excel V / V+)

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified flat vascular patch; congenital. · Reference image search: Wikimedia · Open-i

Primary causes

Congenital capillary malformation — persistent dilated dermal capillaries.
Sporadic somatic mutation (e.g. GNAQ) in most.
Syndromic associations (e.g. Sturge-Weber) in some facial distributions.
Present from birth; not acquired.

Medications

No medication — vascular laser (pulsed-dye is the classic standard; KTP/Nd:YAG also used) lightens the lesion over multiple sessions. Certain facial distributions need medical work-up for syndromic associations.

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
Pulsed-dye / KTP 532 nm	Superficial component; multi-pass, multiple sessions (e.g. fluence titration 2–8 J/cm²).	Best for flat/superficial lesions
Nd:YAG 1064 nm	Deeper/hypertrophic or resistant components.	Thicker lesions; deeper penetration

Guidance only — PWS treatment is a multi-session specialist-style undertaking; confirm device protocol, test-spot, titrate. Refer for syndromic screening where indicated. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Vascular laser — mainstay; many sessions for gradual lightening.
Medical work-up for at-risk facial distributions (e.g. ophthalmology/neurology in Sturge-Weber).
Photoprotection and camouflage as adjuncts.
Set expectations — improvement, rarely complete clearance.

Cautions & contraindications

Screen for syndromic associations in V1/forehead distributions — refer for assessment.
Multiple sessions and partial response — counsel thoroughly.
Darker skin — Nd:YAG with care; PIH risk; test spot.
Periocular involvement — eye protection and caution.

Practitioner review — Port wine stain

P

Aesthetic / dermal-managedKnow when to referInflammatory · Immune-mediated

Psoriasis

A chronic immune-mediated disease with well-demarcated red plaques and silvery scale, classically on elbows, knees and scalp, often with nail and joint involvement. Managed medically; the aesthetic role is recognition, gentle care and referral.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified plaques with silvery scale (elbow/knee/scalp). · Reference image search: Wikimedia · Open-i

Primary causes

Immune-mediated (T-cell) hyperproliferation of keratinocytes.
Genetic predisposition.
Triggers — stress, infection (strep), trauma (Koebner), some drugs, smoking, alcohol.
Associated with psoriatic arthritis and metabolic risk.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical corticosteroids + vitamin D analogues	First-line for plaques	Script
Phototherapy (NB-UVB)	Moderate disease	Medical
Systemics / biologics	Moderate–severe; specialist	Specialist

Treatment modalities to investigate

Recognition and referral for diagnosis and disease/joint assessment.
Gentle, barrier-supportive skincare; emollients.
Avoid skin trauma (Koebner) — caution with procedures over plaques.

Cautions & contraindications

Koebner phenomenon — trauma (microneedling, aggressive procedures) can induce plaques; avoid over lesions.
Do not treat active plaques cosmetically — refer for medical management.
Screen for joint symptoms (psoriatic arthritis) and refer.
Be alert to psychosocial impact and metabolic comorbidity.

Practitioner review — Psoriasis

R

Aesthetic / dermal-managedInflammatory · Vascular

Rosacea

A chronic inflammatory condition of central facial skin presenting as persistent erythema, flushing, telangiectasia, and inflammatory papules and pustules. Subtype-led management; trigger control and barrier support underpin every plan.

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Treatable in-clinic — Vascular laser / IPL for erythema & vessels (e.g. Cutera Excel V / V+)

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

Erythematotelangiectatic, papulopustular and phymatous subtypes. · Reference image search: Wikimedia · Open-i

Primary causes

Neurovascular dysregulation — abnormal flushing and vasodilation.
Immune/inflammatory dysfunction (cathelicidin pathway).
Demodex folliculorum overgrowth (papulopustular).
Impaired skin barrier and triggers (UV, heat, alcohol, spicy food, stress).

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Ivermectin 1% (Soolantra)	Strongest evidence for papulopustular	Script
Metronidazole 0.75–1%	Reliable first-line topical	Script
Azelaic acid 15%	Effective; pregnancy-safe	TGA
Brimonidine 0.5% (Mirvaso)	Temporary erythema reduction only	Script
Doxycycline (incl. 40 mg MR)	Most common oral; sub-antimicrobial dose	Script

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
KTP 532 / Nd:YAG 1064 nm / IPL	Persistent erythema and telangiectasia not addressed by topicals.	Vascular component; 1064 nm safer in darker skin

Guidance only — confirm device protocol, test-spot, titrate. Treats the vascular component; inflammatory disease still needs topical/oral therapy. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Vascular laser / IPL for erythema and telangiectasia.
LED red/near-infrared — anti-inflammatory, barrier-calming.
Barrier-repair skincare — niacinamide, ceramides; avoid harsh actives.
Trigger mapping and mineral photoprotection.

Cautions & contraindications

Brimonidine rebound erythema — can flare worse as it wears off; trial cautiously.
Topical corticosteroids are contraindicated — cause/worsen steroid-induced rosacea.
Aggressive exfoliation, strong actives, heat-based facials flare an impaired barrier.
Doxycycline — photosensitivity; reinforce SPF.
Confirm diagnosis — exclude lupus and other facial dermatoses.

Practitioner review — Rosacea

S

Aesthetic / dermal-managedScarring · Atrophic

Acne scarring

Atrophic & post-acne scarring

Textural scarring after inflammatory acne — atrophic (ice-pick, boxcar, rolling) most commonly, sometimes with erythema or pigment. A major aesthetic concern requiring a combination, scar-type-matched approach over time.

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Treatable in-clinic — Resurfacing & vascular devices: fractional laser, RF microneedling, vascular laser

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified atrophic scar patterns. · Reference image search: Wikimedia · Open-i

Primary causes

Inflammatory acne damage to dermal collagen.
Delayed or inadequate acne treatment.
Genetic and skin-type factors influence scarring.
Picking/manipulation worsens scarring.

Medications

Scars are not drug-treated, but active acne must be controlled first. Residual erythema and pigment respond to topicals/laser; texture needs resurfacing or subcision.

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
Fractional laser / RF microneedling	Stimulate collagen for atrophic texture; series of sessions.	Boxcar/rolling scars; downtime varies
Vascular laser (KTP/Nd:YAG)	Red post-acne scars/erythema.	Erythematous scars

Guidance only — scar-type dictates modality (subcision for tethered rolling scars, TCA CROSS for ice-pick); confirm protocols and manage darker-skin PIH risk. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Control active acne first — treating scars on active acne fails.
Microneedling / fractional laser / RF for atrophic texture.
Subcision for tethered rolling scars; TCA CROSS for ice-pick.
Vascular laser and brighteners for red/pigmented scars.

Cautions & contraindications

Treating over active acne risks worsening — settle the acne first.
Darker skin — PIH risk with resurfacing; conservative settings, test patches.
Isotretinoin timing — coordinate resurfacing with recent isotretinoin use.
Realistic, staged expectations — improvement, not erasure.

Practitioner review — Acne scarring

S

Aesthetic / dermal-managedBenign · Pilosebaceous

Sebaceous hyperplasia

Benign enlargement of sebaceous glands forming soft, yellowish, umbilicated papules, usually on the forehead and cheeks of older or oily-skinned adults. Harmless but cosmetically bothersome; can mimic basal cell carcinoma.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified yellowish umbilicated facial papules. · Reference image search: Wikimedia · Open-i

Primary causes

Benign sebaceous gland enlargement — often age/UV related.
Oily skin and genetic predisposition.
Sometimes associated with ciclosporin therapy.
Increases with age.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical retinoids	May modestly reduce lesions	TGA / Script
Oral isotretinoin	Selected extensive cases; recur after stopping	Specialist

Treatment modalities to investigate

Electrocautery / hyfrecation — common in-clinic removal.
Ablative or pigment/vascular laser in trained hands.
Conservative technique — superficial treatment to avoid scarring.
Reassurance — benign.

Cautions & contraindications

Can mimic basal cell carcinoma — if any doubt, refer for assessment before treating.
Avoid aggressive treatment — risk of scarring/pitting.
Recurrence is common.
Darker skin — pigment change risk; conservative settings.

Practitioner review — Sebaceous hyperplasia

S

Aesthetic / dermal-managedKnow when to referInflammatory · Eczematous

Seborrhoeic dermatitis

A common chronic, relapsing eruption of greasy scale and erythema in sebaceous-rich areas — scalp, nasolabial folds, brows, ears and chest — linked to Malassezia yeast. Easily confused with rosacea or psoriasis.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified nasolabial/brow greasy scale + erythema. · Reference image search: Wikimedia · Open-i

Primary causes

Malassezia yeast interaction with sebum and host response.
Sebaceous-rich skin and seborrhoea.
Triggers — stress, cold/dry weather, immunosuppression.
More prominent in Parkinson's and immunosuppressed patients.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Antifungal (ketoconazole) shampoo/cream	First-line	Pharmacy
Mild topical corticosteroid (short)	Settle inflammation	Pharmacy / Script
Topical calcineurin inhibitors	Steroid-sparing for the face	Script

Treatment modalities to investigate

Antifungal regimen — mainstay (face and scalp).
Gentle, non-stripping skincare.
Manage flares — chronic relapsing course; maintenance.
Distinguish from rosacea/psoriasis to direct treatment.

Cautions & contraindications

Avoid prolonged facial steroids — atrophy and perioral dermatitis risk.
Defer actives/procedures on inflamed skin.
Sudden severe/widespread seborrhoeic dermatitis — consider underlying illness; refer.
Counsel on chronicity — controlled, not cured.

Practitioner review — Seborrhoeic dermatitis

S

Aesthetic / dermal-managedKnow when to referBenign · Keratinocytic

Seborrhoeic keratosis

Extremely common benign growths — warty, 'stuck-on', waxy papules and plaques ranging tan to black, increasing with age. Harmless, but can closely mimic melanoma or pigmented BCC, so confident diagnosis matters before removal.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified 'stuck-on' warty pigmented papules. · Reference image search: Wikimedia · Open-i

Primary causes

Benign keratinocyte proliferation.
Age and genetic predisposition.
Common on trunk, face, scalp.
Not caused by sun alone; not pre-malignant.

Medications

Benign and not requiring treatment; removal (cryotherapy, curettage, shave, laser/electrocautery) is cosmetic — but diagnosis must be confident first.

Treatment modalities to investigate

Cryotherapy / curettage / shave for cosmetic removal.
Dermoscopy / assessment to confirm benign before treating.
Reassurance — benign.
Histology if any diagnostic doubt.

Cautions & contraindications

Can mimic melanoma or pigmented BCC — if a 'seb k' is atypical, changing or uncertain, refer/biopsy before any removal.
Sudden eruption of many lesions (Leser-Trélat) — rare paraneoplastic sign; refer.
Darker skin — pigment-change risk with cryo/laser.
Don't destroy diagnostic tissue if malignancy is possible.

Practitioner review — Seborrhoeic keratosis

S

Aesthetic / dermal-managedBenign · Fibroepithelial

Skin tags

Acrochordon (skin tags)

Soft, benign, pedunculated skin-coloured to brown outgrowths in skin folds — neck, axillae, groin, eyelids. Harmless and very common; simple in-clinic removal once confirmed benign.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified neck/axillary pedunculated tags. · Reference image search: Wikimedia · Open-i

Primary causes

Benign fibroepithelial growth in areas of friction.
Associations — obesity, insulin resistance, pregnancy, age.
Genetic predisposition.
Friction in skin folds contributes.

Medications

No medication — removal by snip excision, cryotherapy or electrocautery once confirmed benign.

Treatment modalities to investigate

Snip excision — quick and effective for most.
Cryotherapy / electrocautery alternatives.
Confirm benign before removal.
Note metabolic associations — many tags may prompt general health advice.

Cautions & contraindications

Confirm diagnosis — pigmented or atypical lesions are not tags; refer if unsure.
Eyelid lesions — careful technique near the eye.
Bleeding/anticoagulants — counsel and manage haemostasis.
Sterile technique to avoid infection.

Practitioner review — Skin tags

S

Aesthetic / dermal-managedVascular · Benign

Spider naevus

Spider naevus (spider angioma)

A benign vascular lesion with a central arteriole and radiating fine vessels that blanches with central pressure. Common and usually solitary; multiple lesions can signal a systemic cause worth noting. A neat KTP-laser target.

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Treatable in-clinic — Vascular laser: KTP 532 nm / Nd:YAG 1064 nm (e.g. Cutera Excel V / V+)

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified central-vessel lesion with radiating capillaries. · Reference image search: Wikimedia · Open-i

Primary causes

Benign dilated central arteriole with radiating capillaries.
Common solitary lesions in children and adults.
Multiple lesions — pregnancy, oestrogen, or liver disease.
Idiopathic in most isolated cases.

Medications

No medication — treated by vascular laser targeting the central feeding vessel; electrosurgery is an alternative.

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
KTP 532 nm	Target the central arteriole; moderate fluence to blanch.	Superficial facial lesions; I–IV
Nd:YAG 1064 nm	Resistant or deeper lesions.	Deeper feeding vessel; darker skin

Guidance only — confirm device protocol, test-spot, titrate to clearance of the central vessel. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Vascular laser targeting the central vessel.
Electrosurgery of the central arteriole as an alternative.
Note multiple lesions — consider systemic cause; review history.
Reassurance for typical solitary lesions.

Cautions & contraindications

Multiple spider naevi — consider liver disease/oestrogen excess; take a history and refer if indicated.
Fitzpatrick V–VI / tanned skin — prefer 1064 nm, lower fluence, test spot.
Recurrence if the central vessel is incompletely treated.
Post-care — transient purpura; photoprotection.

Practitioner review — Spider naevus

S

Recognise & referMalignant · Keratinocytic

Squamous cell carcinoma

Squamous cell carcinoma (SCC)

A common skin cancer arising from keratinocytes — a scaly, tender, sometimes ulcerated or rapidly growing lesion on sun-exposed skin. Can metastasise if neglected. Recognise and refer urgently; never a cosmetic target.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

Scaly/ulcerated lesion; use public-domain oncology sources. · Reference image search: Wikimedia · Open-i · NCI Visuals Online

Primary causes

Cumulative UV exposure — the principal cause; often arises in field damage/AK.
Fair skin, older age, immunosuppression (esp. transplant recipients).
Chronic wounds/scars and HPV in some.
Higher metastatic risk on lip/ear and in immunosuppressed.

Recognise & refer

A scaly, tender, ulcerating or rapidly growing lesion on sun-exposed skin may be an SCC — refer urgently for biopsy. Cosmetic treatment is contraindicated until malignancy is excluded.

Medications

Diagnosis is by biopsy; treatment (excision, Mohs, radiotherapy) is medical/surgical. The practitioner role is recognition and urgent referral.

Clinical approach & referral

Recognition and urgent referral for biopsy.
Photoprotection and skin-check advocacy.
Surveillance — high risk of further skin cancers.

Cautions & contraindications

Never treat a suspicious scaly/ulcerated/rapidly growing lesion cosmetically — refer.
Tender, bleeding, non-healing lesions on sun-damaged skin are red flags.
Lip and ear lesions — higher-risk sites; prompt referral.
Document and direct to medical care without delay.

Practitioner review — Squamous cell carcinoma

S

Aesthetic / dermal-managedScarring · Dermal

Striae (stretch marks)

Striae distensae

Linear dermal scars from rapid skin stretching — red-purple when new (striae rubra), fading to white (striae alba). Common with growth, pregnancy and weight change. Best results come from treating early; mature white striae are harder to improve.

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Treatable in-clinic — Vascular & resurfacing devices: vascular laser (red striae), fractional laser / RF / microneedling

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified striae rubra/alba. · Reference image search: Wikimedia · Open-i

Primary causes

Rapid skin stretching — growth spurts, pregnancy, weight change, bodybuilding.
Hormonal factors — corticosteroids, Cushing's.
Genetic predisposition.
Dermal collagen/elastin disruption.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical retinoids	May improve early striae (avoid in pregnancy)	TGA / Script

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
Vascular laser (KTP/Nd:YAG/PDL)	Reduce redness of early striae rubra.	Best window — newer, red striae
Fractional laser / RF microneedling	Texture/collagen for mature striae alba.	Modest improvement; multiple sessions

Guidance only — early (red) striae respond best; confirm device protocol, test-spot, and manage darker-skin PIH risk. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Treat early — striae rubra respond far better than white striae.
Vascular laser for the red phase.
Microneedling / fractional laser / RF for texture.
Topical retinoids (non-pregnant) as an adjunct.

Cautions & contraindications

Mature white striae — limited improvement; set realistic expectations.
Darker skin — PIH risk with resurfacing; conservative settings, test patches.
Pregnancy — avoid retinoids and elective procedures.
New striae with hypertension/easy bruising — consider Cushing's; refer.

Practitioner review — Striae (stretch marks)

T

Aesthetic / dermal-managedKnow when to referInfective · Fungal

Tinea (fungal infection)

Dermatophytosis (tinea)

A superficial dermatophyte fungal infection — ring-shaped scaly plaques with central clearing (tinea corporis), or involving the face, feet, groin or nails. Frequently mistaken for eczema or other rashes; steroids alone make it worse.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified annular scaly plaque with central clearing. · Reference image search: Wikimedia · Open-i

Primary causes

Dermatophyte fungi — skin-to-skin, animal or fomite/soil spread.
Warm, moist conditions and occlusion.
Shared facilities/equipment and contact sports.
Immunosuppression increases susceptibility.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical antifungals	Localised infection	Pharmacy
Oral antifungals	Extensive, nail or scalp involvement	Script

Treatment modalities to investigate

Confirm fungal cause — scraping/culture if unclear before treating.
Antifungal therapy — topical or oral by extent/site.
Hygiene and reduce spread — avoid sharing, treat contacts/pets.
Avoid procedures over active infection.

Cautions & contraindications

Do not use topical steroids alone — 'tinea incognito' worsens and obscures the rash.
Don't treat over active tinea — defer cosmetic procedures.
Nail and scalp tinea need oral therapy — refer.
Recurrent/widespread infection — consider immunosuppression; refer.

Practitioner review — Tinea (fungal infection)

U

Aesthetic / dermal-managedKnow when to referInflammatory · Allergic

Urticaria (hives)

Urticaria

Transient, itchy weals (hives) from dermal mast-cell histamine release — individual lesions lasting under 24 hours. Acute or chronic; usually managed with antihistamines. Angioedema or systemic features are a medical emergency.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified weals/hives. · Reference image search: Wikimedia · Open-i

Primary causes

Mast-cell histamine release — allergic or non-allergic.
Triggers — foods, drugs, infection, insect stings, physical (pressure, cold, heat).
Chronic spontaneous urticaria — often idiopathic/autoimmune.
Can be provoked by some products/procedures.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Non-sedating antihistamines	First-line; up-dosing under medical guidance	OTC / Script
Short oral corticosteroids	Severe acute flares (medical)	Script
Omalizumab	Refractory chronic urticaria; specialist	Specialist

Treatment modalities to investigate

Identify and avoid triggers where possible.
Antihistamine therapy as the mainstay.
Defer procedures during active urticaria.
Refer chronic or refractory cases.

Cautions & contraindications

Angioedema, lip/tongue/throat swelling, breathing difficulty or anaphylaxis — medical emergency; call for help.
Do not perform elective procedures during a flare.
Note any procedure/product as a possible trigger.
Chronic urticaria (>6 weeks) — refer for work-up.

Practitioner review — Urticaria (hives)

V

Aesthetic / dermal-managedVascular · Benign

Venous lake

A soft, compressible, dark blue-purple papule of dilated venules, typically on the lip, ear or face of older, sun-exposed adults. Benign, but should be distinguished from pigmented lesions; an excellent Nd:YAG laser target.

⚡

Treatable in-clinic — Vascular laser: Nd:YAG 1064 nm (e.g. Cutera Excel V / V+)

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified blue-purple compressible lip/ear papule. · Reference image search: Wikimedia · Open-i

Primary causes

Dilated venules in sun-damaged dermis.
Chronic UV exposure and ageing.
Common on the lower lip and ears.
Benign; compressible (helps distinguish from pigmented lesions).

Medications

No medication — venous lakes are a classic long-pulsed Nd:YAG 1064 nm target; electrosurgery is an alternative for small lesions.

Laser / energy-device approach

Wavelength	Typical published starting parameters	Clinical note
Nd:YAG 1064 nm	Long-pulsed, higher fluence to coagulate the venous channel; often 1–2 sessions.	Excellent for lip/facial venous lakes

Guidance only — confirm device protocol, test-spot, titrate to lesion darkening/flattening without epidermal injury. Counsel on transient swelling, especially on the lip. Full parameters and sources are in the companion reference document.

Treatment modalities to investigate

Long-pulsed Nd:YAG — the modality of choice.
Electrosurgery for small lesions.
Confirm benign (compressible) before treating.
Photoprotection for sun-damaged skin.

Cautions & contraindications

Distinguish from pigmented lesions/melanoma — if non-compressible or atypical, refer before treating.
Lip swelling is common post-treatment — counsel.
Fitzpatrick V–VI — Nd:YAG with care; test spot.
Anticoagulants — counsel on bruising.

Practitioner review — Venous lake

V

Aesthetic / dermal-managedKnow when to referInfective · Viral

Viral warts (verrucae)

Verrucae (HPV warts)

Benign HPV-induced epidermal growths — common warts, plantar verrucae and flat warts — that can spread by contact and autoinoculation. Often self-limiting; relevant because shaving/procedures over warts spread them.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified common/plantar warts. · Reference image search: Wikimedia · Open-i

Primary causes

Human papillomavirus (HPV) — skin-to-skin and fomite spread.
Autoinoculation — scratching, shaving, picking.
Breaks in the skin and moist environments (plantar).
More persistent in immunosuppressed patients.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical salicylic acid	First-line for common/plantar warts	OTC
Cryotherapy	Common clinic treatment	Medical
Other (cantharidin, immunotherapy)	Resistant cases	Medical / Specialist

Treatment modalities to investigate

Salicylic acid ± cryotherapy — mainstays; persistence required.
Avoid shaving/waxing/procedures over warts — prevents spread.
Reassurance — many resolve spontaneously, especially in children.
Refer resistant, facial, genital or extensive warts.

Cautions & contraindications

Do not perform cosmetic procedures over warts — autoinoculation and spread.
Genital warts — refer for appropriate management/STI care.
Immunosuppressed or rapidly changing lesions — refer.
Infection control — contagious; avoid cross-contamination.

Practitioner review — Viral warts (verrucae)

V

Aesthetic / dermal-managedKnow when to referPigmentary · Autoimmune

Vitiligo

An autoimmune loss of melanocytes causing well-defined depigmented (milk-white) patches, often symmetrical and on the hands, face and body folds. Benign but psychologically significant; managed medically, with cosmetic camouflage as support.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified symmetrical depigmented patches. · Reference image search: Wikimedia · Open-i

Primary causes

Autoimmune melanocyte destruction.
Genetic predisposition; associated autoimmune disease (thyroid).
Koebner phenomenon — depigmentation at sites of trauma.
Triggers can include skin injury and stress.

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Topical corticosteroids / calcineurin inhibitors	First-line to re-pigment	Script
Phototherapy (NB-UVB)	Widespread disease	Medical
Topical JAK inhibitors	Emerging therapy; specialist	Specialist

Treatment modalities to investigate

Refer for medical management — best re-pigmentation results come early.
Sun protection of depigmented skin (no melanin protection).
Cosmetic camouflage / self-tan as supportive options.
Screen for associated autoimmune disease.

Cautions & contraindications

Koebner phenomenon — avoid skin-traumatising procedures over/near lesions.
Depigmented skin burns easily — strict photoprotection.
Significant psychosocial impact — manage sensitively; refer.
Avoid procedures that may trigger new patches in active disease.

Practitioner review — Vitiligo

X

Aesthetic / dermal-managedBarrier · Dermatitis

Xerosis (dry skin)

Xerosis cutis

Dry, rough, sometimes scaly or itchy skin from a compromised barrier and reduced hydration. Extremely common, worse in winter and with age; foundational to address before actives or procedures, and a marker of barrier health.

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Clinical example

De-identified, licence-cleared

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Close-up / detail

Add from sources at right

De-identified dry/scaly skin (shins/arms). · Reference image search: Wikimedia · Open-i

Primary causes

Impaired skin barrier and reduced natural moisturising factors.
Environmental — low humidity, cold, wind, hot water, over-washing.
Age — reduced lipids and sebum.
Aggravators — harsh actives/cleansers, some medical conditions (hypothyroid, diabetes, renal).

Clinically proven & TGA-registered medications

Agent	Class / clinical use	Status
Emollients / humectants	Foundation of management (urea, glycerin, ceramides)	OTC
Mild topical steroid (short)	If secondary eczematous change	Pharmacy / Script

Treatment modalities to investigate

Barrier repair — regular emollients, gentle cleansing, lukewarm water.
Reduce irritants — pause harsh actives until restored.
Humectants + occlusives for lasting hydration.
Optimise barrier before procedures/actives.

Cautions & contraindications

Treat dryness before strong actives/procedures — impaired barrier irritates easily.
Severe, sudden or treatment-resistant xerosis — consider systemic cause (thyroid, renal); refer.
Avoid over-exfoliation.
Itch with no rash — exclude systemic causes if persistent.

Practitioner review — Xerosis (dry skin)