📋 Key Information Summary
- A systematic approach to skin problems begins with accurate terminology — describe lesions by type (primary morphology), configuration, colour, and distribution before considering a diagnosis.
- Primary lesions include macule, papule, nodule, plaque, vesicle, bulla, pustule, wheal, and patch; secondary lesions include scale, crust, erosion, ulcer, excoriation, lichenification, and atrophy.
- The diagnostic approach follows a structured sequence: history (onset, duration, symptoms, triggers, medications, atopy, travel, contacts) → morphology description → distribution pattern → differential diagnosis → targeted investigation.
- Distribution is a powerful diagnostic clue: sun-exposed areas suggest photodermatoses; flexural surfaces suggest atopic or seborrhoeic dermatitis; extensor surfaces suggest psoriasis; dermatomal distribution suggests herpes zoster.
- The "SCALP" mnemonic (Site, Colour, Arrangement, Lesion type, Pathology) helps structure clinical description and differential generation.
- Common dermatological conditions in Australian primary care include eczema/atopic dermatitis, psoriasis, acne vulgaris, contact dermatitis, tinea, cellulitis, skin cancers (BCC, SCC, melanoma), urticaria, and rosacea.
- Australian skin cancer rates are the highest globally — a total-body skin examination should be considered in high-risk patients (fair skin, outdoor occupation, immunosuppression, prior skin cancer).
- Dermoscopy (polarised light dermatoscopy) is an essential primary-care tool for pigmented lesion assessment; training via the College of Dermoscopy (RACGP) programme is recommended.
- When in doubt, incisional or excisional biopsy with histopathology is the gold standard for uncertain diagnoses; punch biopsy (3–4 mm) is appropriate for most inflammatory and neoplastic skin conditions.
- Referral indications include: suspected melanoma or aggressive skin cancer, Stevens-Johnson syndrome / toxic epidermal necrolysis, widespread blistering disorders, diagnostic uncertainty after initial workup, and conditions refractory to first-line therapy.
- Aboriginal and Torres Strait Islander peoples have distinct dermatological disease profiles — higher rates of scabies, skin sores (impetigo/pyoderma), tinea, and crusted scabies, particularly in remote communities; culturally safe assessment and treatment are essential.
- Topical corticosteroids remain the mainstay of inflammatory skin disease treatment; use the lowest effective potency for the shortest duration, and match potency to site (low potency for face and flexures, moderate–high for body/extremities).
Introduction & Australian Epidemiology
Skin conditions are among the most common reasons for presentation to Australian general practice, accounting for approximately 15–20% of all consultations. The Australian Institute of Health and Welfare (AIHW) estimates that more than 4 million Australians are affected by a skin condition at any given time. Dermatological complaints span the full spectrum from benign self-limiting conditions (e.g., viral exanthems, contact dermatitis) to life-threatening emergencies (e.g., Stevens-Johnson syndrome, necrotising fasciitis, melanoma).
Australia has the highest incidence of skin cancer in the world. Each year, approximately 2,000 Australians die from skin cancer, and over 16,000 new melanomas and 800,000+ non-melanoma skin cancers (NMSC) are treated annually. The direct healthcare cost exceeds billion per annum. The majority of NMSC (basal cell carcinoma and squamous cell carcinoma) and a significant proportion of melanomas are diagnosed and initially managed in primary care.
In addition to neoplastic disease, inflammatory and infectious skin conditions impose a substantial burden. Atopic dermatitis affects approximately 10–15% of Australian children, with significant impact on quality of life, sleep, and school attendance. Psoriasis affects approximately 2–3% of the adult population. Eczema, acne, and rosacea together account for a large proportion of chronic dermatological management in general practice.
A systematic, structured approach to the diagnosis and management of skin problems is essential. This article provides a framework for: (1) standardised descriptive terminology for skin lesions, (2) a logical diagnostic algorithm, (3) recognition of distribution patterns as diagnostic clues, and (4) an overview of common dermatological conditions encountered in Australian primary care, including management principles and referral criteria.
Australian skin cancer burden: Australia and New Zealand have the highest age-standardised melanoma incidence globally (approximately 50 per 100,000 per year). All primary care clinicians should be competent in skin cancer detection and dermoscopy basics. Refer any suspicious pigmented lesion or non-healing skin lesion for biopsy without delay.
Terminology of Skin Lesions
Accurate description of skin lesions using standardised dermatological terminology is the foundation of clinical diagnosis. Lesions are classified as primary (arising on normal skin, representing the initial pathological change) and secondary (resulting from evolution of primary lesions, external factors, or healing).
Primary Lesions
| Lesion Type | Definition | Size | Example Conditions |
|---|---|---|---|
| Macule | Flat, circumscribed area of colour change; not palpable, <1 cm | <1 cm | Freckle, café-au-lait macule, petechiae (non-blanching), vitiligo |
| Patch | Flat, circumscribed area of colour change; not palpable, ≥1 cm | ≥1 cm | Port-wine stain, vitiligo (large), eczematous patch, pityriasis alba |
| Papule | Solid, elevated, palpable lesion; <1 cm diameter | <1 cm | Acne comedone, wart (verruca), insect bite, molluscum contagiosum, lichen planus |
| Plaque | Elevated, flat-topped, palpable lesion; ≥1 cm diameter (confluence of papules) | ≥1 cm | Psoriasis plaque, eczematous plaque, mycosis fungoides |
| Nodule | Solid, elevated, palpable lesion; deeper than papule (extends into dermis or subcutis); <2 cm | Variable (<2 cm) | Dermatofibroma, lipoma, erythema nodosum, basal cell carcinoma (nodular) |
| Vesicle | Small, fluid-filled, elevated lesion with translucent content; <1 cm | <1 cm | Herpes simplex, varicella, herpes zoster, dyshidrotic eczema (pompholyx) |
| Bulla | Large, fluid-filled, elevated lesion; ≥1 cm | ≥1 cm | Bullous pemphigoid, pemphigus vulgaris, bullous impetigo, friction blister, SJS/TEN |
| Pustule | Elevated, pus-filled lesion (may be follicular or non-follicular) | Variable | Acne pustule, folliculitis, impetigo, pustular psoriasis, acute generalised exanthematous pustulosis (AGEP) |
| Wheal | Firm, transient, oedematous papule or plaque due to dermal oedema; pruritic; resolves within hours | Variable | Urticaria, insect bite reaction |
| Cyst | Encapsulated, fluid- or semisolid-filled cavity within the dermis or subcutis | Variable | Epidermoid (sebaceous) cyst, pilar cyst, dermoid cyst |
Secondary Lesions
| Lesion Type | Definition | Example Conditions |
|---|---|---|
| Scale | Visible flakes of stratum corneum (desquamation) | Psoriasis, eczema, tinea, pityriasis rosea, ichthyosis, seborrhoeic dermatitis |
| Crust | Dried serum, blood, or purulent exudate on the skin surface | Impetigo (honey-coloured crust), eczema (exudative), herpes (dried vesicles) |
| Erosion | Loss of epidermis only (does not extend below basement membrane); heals without scarring | Eczema (excoriated), erosive lichen planus, candidal intertrigo |
| Ulcer | Full-thickness loss of epidermis and at least part of dermis; heals with scarring | Venous leg ulcer, squamous cell carcinoma, pyoderma gangrenosum, pressure injury, melanoma (amelanotic) |
| Excoriation | Linear erosion caused by scratching (self-inflicted) | Atopic dermatitis, scabies, neurotic excoriation, arthropod bite reactions |
| Lichenification | Thickened skin with accentuated skin markings from chronic rubbing/scratching | Chronic atopic dermatitis, lichen simplex chronicus |
| Atrophy | Thinning of the skin (epidermis and/or dermis); may show telangiectasia | Topical corticosteroid atrophy, striae, lichen sclerosus, ageing skin |
| Scar | Fibrous tissue replacing normal skin after dermal injury | Hypertrophic scar, keloid, acne scarring, surgical scar |
| Fissure | Linear crack or slit in the skin (may extend into dermis) | Cracked heels, angular cheilitis, chronic hand eczema, tinea pedis |
Additional Descriptive Terms
- Configuration/Arrangement: grouped, linear, annular (ring-shaped), serpiginous, dermatomal, Koebner phenomenon (lesions along lines of trauma), satellite lesions
- Colour: erythematous (red), hyperpigmented, hypopigmented, violaceous (purple), dusky (suggesting vasculitis or necrosis), yellow (xanthoma, necrosis), blue (blue naevus, dermal melanocytosis)
- Surface change: smooth, rough, verrucous (warty), velvety, shiny, umbilicated (central depression, e.g., molluscum contagiosum)
- Blanching: pressing with a glass slide (diascopy) — non-blanching purpura indicates extravascular blood (vasculitis, meningococcaemia, thrombocytopaenia); blanching erythema indicates vasodilatation
SCALP mnemonic for dermatological description: Site (anatomical location), Colour, Arrangement (grouped, linear, annular), Lesion type (primary and secondary morphology), Pathology/Pattern (differential diagnosis generated from the above). This structured approach ensures no key feature is missed.
Diagnostic Approach to Skin Problems
A systematic diagnostic approach to skin conditions involves four sequential steps: history, morphology description, pattern recognition (distribution + morphology), and targeted investigation. This approach minimises diagnostic error and reduces unnecessary referrals.
Step 1: History
A thorough history narrows the differential before the patient undresses. Key elements include:
- Onset and duration: Acute (<6 weeks) vs chronic (>6 weeks); sudden vs gradual onset
- Initial morphology: What did it start as? (e.g., "started as a small red bump" → papule → evolution to vesicle suggests herpes)
- Symptoms: Pruritus (eczema, urticaria, scabies), pain (herpes zoster, cellulitis), burning (contact dermatitis), asymptomatic (many skin cancers, psoriasis in some cases)
- Triggers and aggravating factors: Sun exposure, heat, cold, water, specific substances, foods, medications (new or changed), stress
- Past medical history: Atopy (asthma, hay fever, eczema), autoimmune conditions, immunosuppression, organ transplant
- Medication history: New medications (drug eruptions typically 7–14 days after initiation), long-term corticosteroids, immunosuppressants
- Occupational and social history: Outdoor worker (skin cancer risk), chemical exposures (occupational contact dermatitis), gardening (sporotrichosis), animals (zoonoses)
- Travel history: Tropical regions (cutaneous larva migrans, leishmaniasis, myiasis)
- Contacts and family history: Scabies (household contacts), atopic dermatitis, psoriasis, skin cancer
Step 2: Morphology Description
Using the terminology described in the section above, describe all lesions systematically:
- Identify primary and secondary lesion types
- Note colour, size, shape, surface texture, borders (well-defined vs ill-defined)
- Test blanching with diascopy (glass slide or transparent cap) — non-blanching = purpura (haemorrhage)
- Palpate: assess induration, fluctuance, tenderness, temperature
Step 3: Distribution and Pattern Recognition
Distribution (see next section in detail) is often the single most informative diagnostic feature. Note:
- Symmetrical vs asymmetrical
- Sun-exposed vs covered skin
- Flexural vs extensor
- Dermatomal, linear, or scattered
- Mucosal involvement (oral, genital, conjunctival) — always examine mucous membranes
- Nail and hair changes (pitting, onycholysis, alopecia) — always examine nails and scalp
Step 4: Investigations
When history and examination are insufficient to establish a diagnosis, targeted investigations are employed:
Essential
Skin scraping / KOH preparation
For suspected fungal infection (tinea, candida). Scrape active edge of lesion, mount in 10–20% KOH, examine for hyphae. Available in most Australian GP practices. No MBS item specific; included in consultation.
Available
Skin swab (MC&S, viral PCR)
Bacterial culture for impetigo, cellulitis, wound infections. Viral PCR swab for suspected herpes simplex or zoster (vesicle base unroofing). Available in all Australian pathology laboratories.
Available
Skin biopsy (punch, shave, excisional)
Gold standard for uncertain diagnoses. Punch biopsy (3–4 mm) for inflammatory and neoplastic conditions. Shave biopsy for raised superficial lesions. Excisional biopsy for suspected melanoma with 2 mm clinical margin. MBS Item 30071 (punch biopsy) and 30072 (excisional biopsy). Refer to dermatologist or experienced GP for biopsy.
Available
Dermoscopy
Polarised or non-polarised dermoscopy significantly improves sensitivity and specificity for melanoma detection (meta-analysis sensitivity ~90%). Recommended for all pigmented lesion assessments. RACGP Certificate of Dermoscopy training available. No specific MBS item; included in consultation.
Available
Patch testing (allergen series)
For suspected allergic contact dermatitis when allergen is not identified by history. Standard series (TRUE Test or extended European/Australian series). Available at dermatology clinics and some specialised GP practices. Requires 48- and 96-hour readings. MBS Item 13200 series.
Specialist
Wood's lamp examination
UV-A light (365 nm) — useful for tinea capitis (Microsporum species fluoresce green), erythrasma (coral-red fluorescence due to Coproporphyrin III), and vitiligo (enhanced contrast). Available in dermatology clinics.
Specialist
Direct immunofluorescence (DIF)
For suspected autoimmune blistering diseases (pemphigus, pemphigoid) and vasculitis. Requires perilesional skin biopsy in Michel's transport medium. Refer to dermatopathology laboratory.
Available
Skin scrapings for scabies (mineral oil mount)
Apply mineral oil to burrow, scrape with scalpel blade, mount on slide. Examine for mites, eggs, or faecal pellets (scybala). Sensitivity ~50%; negative result does not exclude scabies. Clinical diagnosis is often sufficient.
Red-Flag Features Requiring Urgent Referral
Urgent dermatological emergencies — refer to hospital or specialist immediately:
- Stevens-Johnson syndrome / Toxic Epidermal Necrolysis (SJS/TEN): Widespread mucosal erosions, skin pain out of proportion to appearance, positive Nikolsky sign, blistering with epidermal detachment >10% BSA (TEN). Medical emergency — transfer to burns unit.
- Necrotising fasciitis: Rapidly spreading erythema, disproportionate pain, crepitus, skin necrosis, systemic toxicity. Surgical emergency.
- Purpura fulminans / meningococcal purpura: Non-blanching purpura in an unwell patient, particularly with fever and haemodynamic instability.
- Acute generalised exanthematous pustulosis (AGEP): Acute onset of hundreds of small non-follicular pustules on erythematous base, fever, leucocytosis — usually drug-related.
- Angioedema with airway compromise: Swelling of lips, tongue, oropharynx — treat as anaphylaxis if acute.
Distribution of Rashes — Diagnostic Clues
Distribution is often the most powerful clue to dermatological diagnosis. Combining distribution with morphology and history generates a focused differential. The following tables summarise characteristic distributions and associated conditions.
Distribution by Anatomical Site
| Distribution | Typical Conditions | Key Distinguishing Features |
|---|---|---|
| Flexural (antecubital fossae, popliteal fossae, neck folds, wrists) | Atopic dermatitis, seborrhoeic dermatitis, intertrigo (candidal), inverse psoriasis, erythrasma | Atopic eczema: lichenification, excoriations, xerosis. Seborrhoeic: greasy yellowish scale. Candidal: satellite pustules. Inverse psoriasis: smooth erythematous plaques without scale. |
| Extensor (elbows, knees, sacrum, scalp) | Psoriasis (chronic plaque), lichen planus (wrists, ankles), atopic dermatitis (in infants) | Psoriasis: well-demarcated silvery-scaled plaques, nail pitting/onycholysis. Lichen planus: violaceous flat-topped papules, Wickham's striae. |
| Sun-exposed (face, V of chest, dorsal hands/forearms, upper back) | Solar keratoses, BCC, SCC, melanoma, polymorphic light eruption (PMLE), lupus (acute rash), rosacea, drug-induced photosensitivity | PMLE: papules/vesicles appearing hours to days after sun exposure in spring/summer, spares habitually exposed areas (e.g., under chin). Solar keratoses: rough, sandpaper-like patches on chronically sun-damaged skin. |
| Face | Acne vulgaris, rosacea, seborrhoeic dermatitis, perioral dermatitis, contact dermatitis, lupus (malar rash), herpes simplex | Rosacea: centrofacial erythema, papules/pustules, telangiectasia, flushing, no comedones. Perioral dermatitis: papules around mouth with perioral sparing. Acne: comedones + inflammatory papules/pustules. |
| Scalp | Seborrhoeic dermatitis (dandruff), psoriasis (scalp plaques), tinea capitis, alopecia areata, discoid lupus | Seborrhoeic: greasy scale, mild erythema. Psoriasis: well-demarcated thick plaques, often extends to forehead (corona psoriasica). Tinea capitis: alopecia with broken hairs, scaling — predominantly in children. |
| Hands and feet | Contact dermatitis (irritant and allergic), tinea manuum/pedis, dyshidrotic eczema (pompholyx), palmoplantar pustulosis, scabies (web spaces), secondary syphilis | Dyshidrotic eczema: deep-seated vesicles on palms and lateral fingers. Scabies: burrows in finger web spaces, wrists. "One hand, two feet" = tinea manuum + pedis (two feet, one hand syndrome). |
| Dermatomal (unilateral, follows a dermatome) | Herpes zoster (shingles), dermatomal drug eruption (rare) | Herpes zoster: grouped vesicles on erythematous base in a dermatomal distribution, typically unilateral, pain may precede rash by 48–72 hours. Most common: thoracic (T3–L2), trigeminal (V1 > V2 > V3). |
| Generalised / widespread | Viral exanthem, drug eruption, urticaria, scabies (widespread), secondary syphilis, guttate psoriasis, eczema herpeticum, SJS/TEN | Drug eruption: usually 7–14 days after new drug; morbilliform pattern most common. Viral exanthem: prodrome (fever, malaise), then eruption. Guttate psoriasis: small "drop-like" papules, often post-streptococcal. |
| Trunk and limbs (annular/ring-shaped) | Tinea corporis (ringworm), granuloma annulare, erythema migrans (Lyme — rare in Australia), annular psoriasis, pityriasis rosea | Tinea corporis: annular plaque with active scaly advancing border and central clearing. Granuloma annulare: firm, non-scaly, annular flesh-coloured or pink papules. Pityriasis rosea: herald patch followed by secondary eruption along skin lines ("Christmas tree" pattern). |
| Perineal / genital | Genital herpes, condylomata (HPV), candidiasis, lichen sclerosus, scabies, psoriasis (inverse), syphilis (chancre), dermatitis | Always consider STIs in genital dermatosis. Lichen sclerosus: porcelain-white atrophic plaques, figure-of-eight pattern around vulva and anus. Genital herpes: painful grouped vesicles that ulcerate. |
Pattern Recognition — Configuration
| Pattern | Description | Suggests |
|---|---|---|
| Annular | Ring-shaped; central clearing with active border | Tinea corporis, granuloma annulare, annular erythema, erythema migrans, subacute cutaneous lupus |
| Linear | Lesions in a straight line | Contact dermatitis (e.g., plant allergy — Rhus dermatitis), linear epidermal naevus, linear IgA disease, dermatitis herpetiformis (extensor surfaces, grouped), insect bite track (cutaneous larva migrans) |
| Grouped / Herpetiform | Clustered lesions | Herpes simplex (grouped vesicles), herpes zoster (grouped vesicles in dermatome), dermatitis herpetiformis |
| Koebner phenomenon | Lesions developing along lines of trauma | Psoriasis, lichen planus, vitiligo, molluscum contagiosum |
| Photodistribution | Affects sun-exposed areas, spares shaded areas (submental, post-auricular, upper eyelid) | PMLE, dermatomyositis (heliotrope rash, Gottron's papules), cutaneous lupus, drug photosensitivity |
Common Dermatological Condition Overview
The following section provides a concise overview of the most common dermatological conditions encountered in Australian primary care, with a focus on key features, first-line management, and referral indications.
1. Atopic Dermatitis (Eczema)
Atopic dermatitis is the most common inflammatory skin disease in Australian children, affecting 10–15% of children under 5 years and approximately 10% of adults. It is characterised by chronic relapsing pruritic eczema with a predilection for flexural surfaces, xerosis (dry skin), and a personal or family history of atopy.
Diagnostic criteria (Hanifin and Rajka): Major criteria — pruritus, typical morphology and distribution, chronic relapsing course, personal/family history of atopy.
Mild
Mild Atopic Dermatitis
Localised areas of dry skin with mild erythema and pruritus. No sleep disturbance. Minimal impact on quality of life.
Setting: General practice
Moderate
Moderate Atopic Dermatitis
Wider distribution of erythematous patches/plaques, excoriations, lichenification. Sleep disturbance. Intermittent flares requiring step-up therapy.
Setting: General practice ± dermatology review
Severe
Severe Atopic Dermatitis
Widespread erythema, lichenification, excoriations, fissuring. Significant sleep disturbance, school/work absenteeism, psychological distress. Eczema herpeticum risk.
Setting: Dermatologist-led care; consider systemic therapy
Management — Eczema
1
Emollients (foundation therapy)
Apply generously (250–500 g/week for adults) at least twice daily and immediately after bathing. Soap-free wash (e.g., QV Wash®, DermaVeen®). Bath oils (e.g., Alpha Keri®, QV Bath Oil®). PBS-listed emollients available on authority prescription for patients with chronic eczema (PBS Item 8510).
2
Topical corticosteroids (anti-inflammatory)
Mild (face/flexures): Hydrocortisone 1% cream (low potency). Moderate (body): Mometasone furoate 0.1% cream (Elocon®) or betamethasone valerate 0.02% (Betnovate®). Severe/acute flares: Clobetasol propionate 0.05% (Dermovate®) — short course (5–7 days) then step down. Apply once daily to affected areas only. Avoid prolonged use on face and flexures. All PBS-listed.
3
Topical calcineurin inhibitors (steroid-sparing)
Tacrolimus ointment 0.03% (children 2–15 years) or 0.1% (adults) — Protopic®. Pimecrolimus 1% cream — Elidel®. For facial and flexural eczema, and as maintenance therapy to prevent flares. Not PBS-subsidised for atopic dermatitis (authority required for some indications). No risk of skin atrophy.
4
Systemic therapy (dermatologist-supervised)
For severe, refractory disease: Dupilumab (Dupixent®) — IL-4/IL-13 monoclonal antibody, PBS Authority Required for patients ≥12 years with severe atopic dermatitis not controlled by topical therapy. Other options: Ciclosporin (short-term), azathioprine, methotrexate (all specialist-initiated).
2. Psoriasis
Psoriasis affects approximately 2–3% of the Australian population. It is a chronic immune-mediated inflammatory condition characterised by well-demarcated, erythematous plaques with silvery-white scale, typically on extensor surfaces (elbows, knees), scalp, sacrum, and nails. Koebner phenomenon is common.
Clinical subtypes: Chronic plaque (most common, ~90%), guttate, inverse, pustular (localised and generalised), erythrodermic.
Psoriasis and comorbidities: Psoriasis is a systemic inflammatory condition. Patients with moderate-to-severe psoriasis have increased risk of cardiovascular disease, metabolic syndrome, psoriatic arthritis (30%), depression, and inflammatory bowel disease. Screen and manage these comorbidities proactively (RACGP / ARA guidelines).
First-line management:
- Emollients and keratolytics: Salicylic acid preparations (e.g., Psoriasin®) for thick plaques; coal tar preparations (e.g., LCD — liquor carbonis detergens); urea cream for scale
- Topical corticosteroids: Moderate-to-potent (e.g., betamethasone dipropionate 0.05%, mometasone 0.1%) — once daily for 2–4 weeks, then taper or alternate with calcipotriol
- Vitamin D analogue: Calcipotriol 50 µg/g ointment (Daivonex®) — twice daily. PBS-listed. Can be combined with betamethasone (Daivobet® / Enstilar® foam). Avoid hypercalcaemia with overuse (>100 g/week in adults)
- Specialist phototherapy: Narrowband UV-B (NB-UVB) — effective for widespread plaque psoriasis and guttate psoriasis. Available in hospital dermatology departments and some private phototherapy centres.
- Systemic therapy (specialist-supervised): Methotrexate (PBS authority), ciclosporin, acitretin, apremilast. Biologic agents: TNF-α inhibitors (adalimumab, etanercept, infliximab), IL-17 inhibitors (secukinumab, ixekizumab, bimekizumab), IL-23 inhibitors (guselkumab, risankizumab, tildrakizumab), IL-12/23 inhibitor (ustekinumab) — all PBS authority required for severe psoriasis.
3. Acne Vulgaris
Acne is the most common skin condition globally and affects up to 85% of adolescents in Australia. Pathogenesis involves pilosebaceous unit dysfunction: follicular hyperkeratinisation, excess sebum production (androgen-driven), Cutibacterium acnes proliferation, and inflammation.
Mild
Comedonal / Mild Inflammatory
Open and closed comedones (blackheads and whiteheads) ± few inflammatory papules. Mainly face.
Setting: General practice; topical therapy
Moderate
Moderate Inflammatory
Multiple inflammatory papules and pustules, comedones, with some nodules. Face ± trunk. Early scarring possible.
Setting: General practice; topical ± oral therapy
Severe
Severe Nodulocystic
Extensive inflammatory nodules, cysts, sinus tracts. Scarring. Significant psychological impact. May involve trunk, back, and buttocks.
Setting: General practice or dermatologist; oral isotretinoin considered
Adapalene
Differin® · Retinoid (topical)
Adult dose
Apply thin layer to affected area once daily at night
Notes
First-line topical retinoid for comedonal and inflammatory acne. Less irritating than tretinoin. Initial worsening possible (6–8 weeks to see benefit). Avoid in pregnancy.
PBS status
✔ PBS General Benefit
Benzoyl Peroxide
Benzac AC® / PanOxyl® · Antimicrobial (topical)
Adult dose
2.5–5% gel/cream to affected area once or twice daily
Notes
First-line antimicrobial for inflammatory acne. No bacterial resistance. Available OTC and on prescription. Can bleach fabrics. May be combined with adapalene (Epiduo®).
PBS status
✔ PBS General Benefit
Doxycycline
Doxy® / Doryx® · Tetracycline antibiotic
Adult dose
50–100 mg PO once or twice daily for 3–6 months
Paediatric dose
≥8 years: 2 mg/kg/day PO (max 100 mg/day)
Notes
First-line oral antibiotic for moderate-to-severe inflammatory acne. Sub-antimicrobial dose (40 mg modified release — Oracea®) effective for anti-inflammatory effect. Photosensitivity common — counsel sun protection.
PBS status
✔ PBS General Benefit
Isotretinoin
Roaccutane® / Oratane® · Oral retinoid
Adult dose
0.5–1 mg/kg/day PO in divided doses with food; cumulative dose target 120–150 mg/kg per course
Duration
Typically 4–8 months per course
Notes
Most effective treatment for severe nodulocystic acne. Absolute teratogen — requires pregnancy prevention programme (two forms of contraception, negative pregnancy test before starting, monthly pregnancy tests). Side effects: dry skin/lips, myalgia, elevated LFTs, hypertriglyceridaemia. Monitor FBC, LFTs, lipids at baseline, 1 month, then every 2–3 months. Prescriber must be registered with Roche pregnancy prevention programme.
PBS status
⚠ PBS Authority Required
4. Contact Dermatitis
Contact dermatitis is categorised as irritant (80% of cases; direct chemical/physical damage) or allergic (20%; Type IV delayed hypersensitivity). Common allergens in Australia include nickel (jewellery, belt buckles), fragrances, preservatives (methylisothiazolinone), rubber accelerators, hair dyes (p-phenylenediamine), and plants.
Management: Identify and avoid causative agent. Short courses of topical corticosteroids for flares. Patch testing (TRUE test or extended series) for recurrent or occupational cases. WorkCover referrals for occupational contact dermatitis are common in Australia.
5. Tinea (Dermatophytosis)
Tinea infections are caused by dermatophyte fungi (Trichophyton, Microsporum, Epidermophyton) and are classified by site:
| Type | Common Species (Australia) | Key Features | First-Line Treatment |
|---|---|---|---|
| Tinea pedis (athlete's foot) | T. rubrum, T. interdigitale | Interdigital (web-space maceration/scale) or moccasin-type (plantar/hyperkeratotic). Pruritic. "Two feet, one hand" syndrome common. | Topical: Terbinafine 1% cream (Lamisil®) once daily for 1–2 weeks. For moccasin-type: oral terbinafine 250 mg daily for 2–4 weeks. |
| Tinea corporis (ringworm) | T. rubrum, M. canis | Annular plaque with active scaly border and central clearing. Pruritic. | Topical: Terbinafine 1% cream for 1–2 weeks. Widespread/recurrent: oral terbinafine 250 mg daily for 2–4 weeks. Oral griseofulvin (especially Microsporum species in children). |
| Tinea cruris (jock itch) | T. rubrum, T. mentagrophytes | Erythematous, scaly plaques in inguinal folds. Spares scrotum (helps differentiate from candidal intertrigo, which involves scrotum). Often bilateral. | Topical: Terbinafine 1% cream for 1–2 weeks. Oral if widespread or recurrent. |
| Tinea capitis | M. canis, T. tonsurans | Predominantly in children. Scaly patch with alopecia and broken hairs ("black dot" pattern for T. tonsurans). Kerion (inflammatory boggy mass) may occur. | Oral antifungal required (topicals ineffective for hair shaft penetration). Griseofulvin: children 10–20 mg/kg/day for 6–8 weeks. Terbinafine: weight-based dosing for 4–6 weeks (Trichophyton better than Microsporum). Refer if kerion present. |
| Tinea unguium (onychomycosis) | T. rubrum (most common) | Thickened, discoloured (white/yellow/brown), brittle nail. Subungual hyperkeratosis. Confirm diagnosis with nail clipping histology/pas stain and culture before treatment. | Oral terbinafine 250 mg daily: fingernails for 6 weeks, toenails for 12–16 weeks. Monitor LFTs. Topical amorolfine 5% nail lacquer (Loceryl®) for mild distal disease only. PBS Authority Required for oral terbinafine in confirmed onychomycosis. |
6. Urticaria
Urticaria (hives) presents as transient wheals (wheal-and-flare) lasting <24 hours per individual lesion, with no residual bruising. Classified as acute (<6 weeks) or chronic (>6 weeks). Acute urticaria is often idiopathic, viral, or allergic (food, drug, insect sting). Chronic spontaneous urticaria (CSU) has an autoimmune basis in approximately 40% of cases.
Anaphylaxis warning: Urticaria accompanied by angioedema, bronchospasm, hypotension, or laryngeal oedema is anaphylaxis — administer IM adrenaline (epinephrine) 0.5 mg (adult) / 0.01 mg/kg (child) into the mid-anterolateral thigh immediately and call 000.
Management:
- Non-sedating antihistamines (first-line): Cetirizine 10 mg daily (Zyrtec®), loratadine 10 mg daily (Claratyne®), or fexofenadine 180 mg daily (Telfast®). All PBS-listed. Up-dosing to 4× standard dose is recommended by international guidelines (EAACI/GA²LEN) for refractory chronic urticaria before adding second-line agents.
- Second-line for CSU: Omalizumab (Xolair®) — anti-IgE monoclonal antibody. PBS Authority Required for chronic spontaneous urticaria refractory to high-dose antihistamines. Dermatologist or immunologist-initiated.
- Short course of oral corticosteroids for severe acute flares: Prednisolone 25–50 mg daily for 3–5 days (adults). Avoid long-term use.
7. Cellulitis and Skin and Soft Tissue Infections
Cellulitis is an acute bacterial infection of the dermis and subcutaneous tissue, typically caused by Streptococcus pyogenes (Group A Strep) and Staphylococcus aureus. Risk factors include lymphoedema, venous insufficiency, tinea pedis (port of entry), skin breaks, obesity, and immunosuppression.
Uncomplicated cellulitis (no purulence)
Flucloxacillin 500 mg PO QDS for 5–7 days
5–7 days (or until erythema resolving + afebrile for 48 h)
Pen allergy: Cefalexin 500 mg PO QDS or clindamycin 450 mg PO TDS
Purulent cellulitis / abscess
I&D first-line + consider TMP/SMX (trimethoprim/sulfamethoxazole) 160/800 mg PO BD
5–7 days
Cover for CA-MRSA in areas of high prevalence (remote NT communities, urban hotspots). Send pus for MC&S.
Severe cellulitis (systemic signs, rapid spread)
Benzylpenicillin 1.2 g IV QDS + flucloxacillin 2 g IV QDS
IV until improving, then oral step-down to complete 10–14 days total
Admit to hospital. Mark advancing border with pen. If not responding in 48–72 h, consider necrotising fasciitis, resistant organism, or alternative diagnosis.
8. Skin Cancer — Australian Context
Australia has the highest rate of skin cancer globally. The three main types are:
- Basal cell carcinoma (BCC): Most common cancer in Australia. Slow-growing, locally invasive, rarely metastasises. Presents as pearly nodule, superficial erosion, or non-healing ulcer. Common on face and trunk. Treat with surgical excision (MBS Item 31359), curettage, cryotherapy, or topical treatments (imiquimod 5% for superficial BCC — Aldara®, PBS Authority).
- Squamous cell carcinoma (SCC): Second most common. Can metastasise. Presents as erythematous, scaly, indurated plaque or nodule; may ulcerate. Actinic keratoses are precursors. Treat with excision (MBS Item 31359). High-risk SCC requires wider margins and may need Mohs micrographic surgery.
- Melanoma: Most lethal skin cancer. Australia: ~16,000 new cases and ~1,300 deaths per year. Recognised using the ABCDE criteria (Asymmetry, Border irregularity, Colour variation, Diameter >6 mm, Evolving). Also note the "ugly duckling" sign (lesion that looks different from surrounding naevi). Any suspicious pigmented lesion requires excisional biopsy with 2 mm clinical margin — do not shave biopsy suspected melanoma. Refer to dermatologist/surgical oncologist. Sentinel lymph node biopsy for staging in lesions ≥0.8 mm Breslow thickness.
Dermoscopy improves melanoma detection: A meta-analysis demonstrates that dermoscopy by a trained clinician increases sensitivity for melanoma detection from ~70% (naked eye) to ~90%. All Australian GPs managing skin lesions should consider undertaking RACGP-accredited dermoscopy training. The "Chaos and Clues" and "Menzies method" are validated Australian dermoscopy algorithms.
9. Rosacea
Rosacea is a chronic inflammatory condition of the face characterised by flushing, persistent centrofacial erythema, papules/pustules, and telangiectasia. It predominantly affects adults aged 30–60 years, and is more common in fair-skinned individuals of Celtic and Northern European descent — a significant proportion of the Australian population.
Subtypes: Erythematotelangiectatic, papulopustular, phymatous (rhinophyma), ocular. Distinguished from acne by the absence of comedones.
First-line management:
- Metrogel® (metronidazole 0.75% gel): Twice daily — anti-inflammatory effect. PBS-listed.
- Azelaic acid 15% gel (Finacea®): Twice daily — anti-inflammatory and anti-keratinisation. PBS-listed.
- Brimonidine gel (Mirvaso® 0.33%): Once daily — alpha-2 agonist causing vasoconstriction for persistent erythema. Not PBS-listed.
- Oral doxycycline 40–100 mg daily for moderate papulopustular rosacea (anti-inflammatory dose). PBS-listed.
- Oral ivermectin and topical ivermectin 1% cream (Soolantra®) — effective for papulopustular rosacea (anti-inflammatory and anti-Demodex). Not PBS-listed.
10. Impetigo (School Sores)
Impetigo is the most common bacterial skin infection in Australian children, caused predominantly by Staphylococcus aureus and Streptococcus pyogenes. Two forms: non-bullous (honey-coloured crusts, most common) and bullous (flaccid blisters, S. aureus exfoliative toxins). Highly contagious — common in tropical and remote communities.
Management: Topical mupirocin 2% ointment (Bactroban®) TDS for 5 days for localised non-bullous impetigo. Oral flucloxacillin (adults 500 mg QDS; children 12.5–25 mg/kg QDS) for 7 days if widespread, systemic signs, or failed topical therapy. For CA-MRSA: TMP/SMX or clindamycin. See ATSI section for endemic impetigo in remote communities.
Topical Corticosteroid Potency Guide
Correct selection of topical corticosteroid potency is fundamental to managing inflammatory skin disease. Use the lowest effective potency for the shortest duration. Match potency to body site: lower potency for thin skin (face, flexures, genitals) and higher potency for thick skin (palms, soles, elbows, knees).
| Potency Class | Representative Agent | Brand | Appropriate Sites |
|---|---|---|---|
| Mild (Group I) | Hydrocortisone 1% | Sigmacort® / DermAid® | Face, flexures, genitals, infants, intertriginous areas |
| Moderate (Group III–IV) | Betamethasone valerate 0.02% | Betnovate® RD | Trunk, limbs, most eczema/psoriasis on body |
| Potent (Group V–VI) | Mometasone furoate 0.1% Betamethasone dipropionate 0.05% |
Elocon® Betnovate® |
Body, limbs, scalp. NOT face or flexures (short-term only) |
| Very potent (Group VII) | Clobetasol propionate 0.05% | Dermovate® | Palms, soles, thick chronic plaques only. Maximum 50 g/week. Short courses only (≤2 weeks). NOT for face or flexures. |
Topical corticosteroid phobia: Many patients and parents fear topical cortosteroids due to misconceptions about skin thinning. Counsel patients that appropriate short-course use of topical corticosteroids on indicated body sites is safe and effective. Emphasise that untreated eczema causes more harm (lichenification, infection, sleep disturbance) than appropriate topical corticosteroid use. Use the term "eczema cream" rather than "steroid" if helpful.
Special Populations
Pregnancy
Physiological skin changes: striae, hyperpigmentation (melasma/chloasma, linea nigra), spider naevi, palmar erythema — all normal.
Specific dermatoses of pregnancy: atopic eruption of pregnancy (most common), polymorphic eruption of pregnancy (PEP — formerly PUPPP), pemphigoid gestationis (bullous, autoantibody-mediated), intrahepatic cholestasis of pregnancy (pruritus without primary rash — check serum bile acids).
Safe topical treatments: Emollients, low-potency topical corticosteroids (hydrocortisone), calamine lotion. Topical tacrolimus appears safe based on limited data but is not officially recommended in pregnancy.
Contraindicated: Retinoids (all — teratogenic), high-potency topical corticosteroids (risk of foetal adrenal suppression with prolonged use), tetracyclines (tooth/bone discolouration), methotrexate (abortifacient/teratogenic).
Safe oral antibiotics: Cephalosporins, erythromycin/azithromycin, penicillins
Paediatrics
Common conditions by age: Neonates — erythema toxicum neonatorum, milia, transient pustular melanosis (all benign). Infants — atopic dermatitis, infantile haemangioma, napkin dermatitis. Children — viral exanthems, molluscum contagiosum, warts, impetigo, tinea capitis.
Atopic dermatitis management: As per adult principles but use lower-potency corticosteroids. Hydrocortisone 1% for face and flexures. Emollients are the mainstay — generous application is critical.
Topical corticosteroid caution: Children have higher body surface area to weight ratio — greater systemic absorption risk. Use mild-to-moderate potency, short courses. Avoid very potent corticosteroids in children.
Impetigo: Very common in children. Topical mupirocin for localised disease; oral antibiotics for widespread disease. Exclude from school/childcare until lesions are treated for >24 hours.
Note: Tinea capitis requires systemic (oral) antifungal therapy — topical agents do not penetrate the hair shaft.
Elderly
Xerosis (dry skin): Extremely common in the elderly. Regular emollient use is the cornerstone of management. Reduce bathing frequency and temperature.
Skin cancer: Highest incidence in elderly Australians. Regular full-body skin checks. Comorbidities may limit surgical options — consider cryotherapy, curettage, topical treatments for superficial BCC/solar keratoses.
Drug eruptions: Polypharmacy increases risk. Common culprits include antibiotics (amoxicillin, sulphonamides), NSAIDs, diuretics, anticonvulsants.
Shingles (herpes zoster): Increased severity and risk of post-herpetic neuralgia in the elderly. Shingrix® (recombinant zoster vaccine) is recommended and funded under the NIP for adults ≥65 years.
Note: Venous eczema and stasis dermatitis are common — assess for chronic venous insufficiency. Compression therapy is the mainstay of treatment.
Immunocompromised
Organ transplant recipients: Dramatically increased risk of SCC (65-fold), BCC, Kaposi sarcoma, and viral warts. Requires regular dermatological surveillance (every 6–12 months).
Biologic therapy patients: Psoriasis patients on biologics may develop paradoxical drug reactions (e.g., eczema-like eruptions on TNF-α inhibitors, new-onset psoriasis on IL-17 inhibitors).
HIV/AIDS: Severe/atypical presentations of common conditions (extensive herpes, widespread molluscum, oral hairy leukoplakia, Kaposi sarcoma, seborrhoeic dermatitis). Consider HIV testing in recurrent or atypical dermatological presentations.
Note: Any non-healing or atypical skin lesion in an immunocompromised patient warrants early biopsy to exclude malignancy or opportunistic infection.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health — Dermatological Considerations
📚 References
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