The Skin, Nails and Lumps

📋 Key Information Summary

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Systematic history — always ask about rash onset (acute <6 weeks vs chronic >6 weeks), distribution, morphology, itch (pruritus), triggers, medications (including OTC and supplements), atopy/family history, and occupational exposures.
Primary lesions are the fundamental building blocks of dermatological diagnosis — macule (<1 cm flat), patch (>1 cm flat), papule (raised <1 cm), nodule (deep >1 cm), vesicle (<0.5 cm fluid-filled), bulla (>0.5 cm fluid-filled), pustule (pus-filled), and plaque (raised >1 cm, flat-topped).
Secondary lesions — scale, crust, erosion, ulcer, fissure, excoriation, lichenification, and atrophy indicate evolution of the primary process, scratching, or chronicity.
Distribution patterns are diagnostic clues: extensor surfaces (dermatitis herpetiformis), sun-exposed areas (lupus, dermatomyositis), flexural (atopic dermatitis), dermatomal (herpes zoster), acral (hand-foot-and-mouth disease).
Blistering eruptions — distinguish tense blisters (bullous pemphigoid, typically elderly) from flaccid blisters (pemphigus vulgaris, Nikolsky sign positive) and grouped vesicles on extensor surfaces (dermatitis herpetiformis, associated with coeliac disease).
Bullous pemphigoid — most common autoimmune blistering disease in Australia; first-line treatment is superpotent topical corticosteroids (clobetasol propionate 0.05%) or oral prednisolone 0.5 mg/kg/day; doxycycline is an alternative first-line.
Pemphigus vulgaris — potentially life-threatening; requires systemic immunosuppression; rituximab is now preferred first-line per 2020 international consensus; oral prednisolone 1–2 mg/kg/day for flares.
Dermatitis herpetiformis — intensely pruritic grouped papulovesicles on extensor surfaces; pathognomonic for coeliac disease; dapsone 50–100 mg daily provides rapid symptom relief; lifelong gluten-free diet is the definitive treatment.
Drug reactions — morbilliform eruption is most common drug rash; always consider SJS/TEN (cut-offaneous ≥10% BSA detachment) in any drug-associated blistering; stop culprit drug immediately and refer urgently to burns/plastics if SJS/TEN suspected.
Nail examination — pitting (psoriasis, alopecia areata), onycholysis (psoriasis, thyrotoxicosis, fungal infection), koilonychia (iron deficiency), leuconychia (trauma, hypoalbuminaemia, heavy metal poisoning), nailfold telangiectasia (dermatomyositis, scleroderma), splinter haemorrhages (endocarditis, vasculitis).
Lump assessment — use a systematic approach: site, size, shape, surface, edge, colour, consistency (soft/firm/hard/fluctuant), compressibility, reducibility, transillumination, tenderness, mobility, and overlying skin changes.
Red-flag features requiring urgent referral: rapidly growing lumps (>50% growth in 1 month), size >5 cm, fixed/deep lesions, constitutional symptoms (weight loss, night sweats), non-healing ulcers, and lesions in high-risk anatomical sites.
Always consider systemic disease — skin signs may indicate malignancy (Sézary syndrome, paraneoplastic pemphigus), autoimmune connective tissue disease (lupus, dermatomyositis), endocrine conditions (Cushing syndrome, acromegaly), or infection (HIV, syphilis, leprosy).
Dermoscopy improves diagnostic accuracy for pigmented lesions (sensitivity >90% when performed by trained practitioners) and is recommended for any suspicious pigmented skin lesion (MBS item 23923 for biopsy with histological examination).

Introduction & Australian Epidemiology

Skin conditions are among the most common reasons for presentation to Australian general practitioners, accounting for approximately 15–20% of all GP consultations nationally. The Australian Institute of Health and Welfare (AIHW) reports that skin cancer remains the most commonly diagnosed cancer in Australia, with over 15,000 melanoma and approximately 980,000 non-melanoma skin cancer (NMSC) diagnoses annually. Australia has one of the highest rates of skin cancer globally, driven by predominantly fair-skinned population demographics, high ambient ultraviolet (UV) radiation indices, and historically high recreational sun exposure.

Dermatological examination is a core clinical skill that extends far beyond the skin. The skin is the largest organ system and serves as a window to systemic disease. A structured approach — combining a thorough history with systematic lesion description, distribution mapping, and targeted examination of nails, hair, and mucous membranes — enables accurate diagnosis and appropriate triage. Lumps and bumps are an extremely common presenting complaint, and a reproducible assessment framework differentiates benign from sinister pathology, guiding the decision to observe, image, biopsy, or refer.

In the Australian context, particular consideration must be given to: (1) high rates of skin cancer requiring vigilant lesion assessment; (2) unique patterns of skin disease in Aboriginal and Torres Strait Islander populations, including high rates of scabies, group A streptococcal skin infections, and rheumatic fever; (3) the impact of occupational sun and chemical exposure in outdoor industries; and (4) the growing burden of atopic dermatitis and psoriasis affecting quality of life across all age groups.

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Australian skin cancer burden: Two in three Australians will be diagnosed with skin cancer by age 70. Any pigmented lesion changing in size, shape, or colour — or any non-healing ulcer — warrants urgent assessment and, where indicated, excisional biopsy under the ABCDE criteria (Asymmetry, Border irregularity, Colour variation, Diameter >6 mm, Evolving).

Dermatological History

A structured dermatological history is the cornerstone of skin diagnosis. Up to 80% of dermatological diagnoses can be made on history alone, with examination serving to confirm the clinical impression. The history should be comprehensive and systematic, capturing the following domains:

Onset and Duration

Acute (<6 weeks) — consider infections (viral exanthem, bacterial cellulitis), allergic drug reactions, urticaria, contact dermatitis.
Chronic (>6 weeks) — consider eczema/atopic dermatitis, psoriasis, autoimmune blistering disease, cutaneous T-cell lymphoma.
Age of onset — childhood onset suggests atopic dermatitis or genetic conditions (e.g., ichthyosis); adult-onset papulosquamous disease favours psoriasis or secondary syphilis.

Morphology and Distribution

Ask the patient to describe the original lesion before any secondary changes (scratching, infection, treatment).
Document distribution using standardised anatomical terms: generalised, localised, flexural, extensor, acral, dermatomal, sun-exposed, or bathing-trunk distribution.
Note symmetry — bilateral symmetric involvement suggests systemic conditions (atopy, drug eruption); unilateral/asymmetric involvement suggests infection, contact, or neoplastic aetiology.

Symptoms

Pruritus (itch) — extremely common; differential includes eczema, urticaria, scabies (especially if worse at night), cholestasis, chronic kidney disease, and polycythaemia vera.
Pain — suggests herpes zoster, erythema nodosum, pyoderma gangrenosum, or malignancy.
Burning/stinging — consider contact dermatitis, rosacea, neuropathic pain (post-herpetic neuralgia).
Asymptomatic — consider malignancy (basal cell carcinoma, melanoma), vitiligo, or early psoriasis.

Triggers and Aggravating Factors

Sun exposure — polymorphic light eruption, lupus erythematosus, solar urticaria, dermatomyositis.
Heat/sweating — cholinergic urticaria, miliaria, folliculitis.
Cold — cold urticaria, Raynaud phenomenon.
Water/aquagenic — aquagenic urticaria, aquagenic pruritus (consider polycythaemia vera).
Pressure/friction — delayed pressure urticaria, lichen simplex chronicus.
Foods — urticaria (IgE-mediated), dermatitis herpetiformis (gluten), oral allergy syndrome.

Drug History

Document all medications — prescription, over-the-counter, complementary medicines, and supplements with exact dates of commencement.
Common culprits: antibiotics (amoxicillin, sulfonamides — morbilliform eruption), ACE inhibitors (lichenoid drug eruption), anticonvulsants (DRESS syndrome with carbamazepine, phenytoin, lamotrigine), diuretics (photosensitivity with thiazides), biologics (psoriasiform eruption with TNF-α inhibitors), and NSAIDs (fixed drug eruption).
Temporal relationship — most drug eruptions occur within 1–3 weeks of starting the offending agent; re-exposure may cause eruption within hours.

Family and Atopic History

Atopic triad — personal or family history of eczema, asthma, and/or allergic rhinitis strongly supports atopic dermatitis.
Psoriasis — 30–40% have a positive family history; HLA-Cw6 is the strongest genetic risk factor.
Autoimmune blistering disease — family clustering is uncommon but HLA associations exist (HLA-DQ2 in dermatitis herpetiformis).
Skin cancer — family history of melanoma, Fitzpatrick skin type I–II, and familial atypical multiple mole melanoma (FAMMM) syndrome increase risk.

Occupational and Environmental Exposure

Outdoor workers — construction, farming, mining, and surf lifesaving: elevated UV exposure with high NMSC and melanoma risk; Safe Work Australia recommends UV protection protocols.
Chemical exposure — cement workers (chromate dermatitis, irritant contact dermatitis), hairdressers (allergic contact dermatitis to paraphenylenediamine), healthcare workers (latex allergy, hand dermatitis).
Animal/soil contact — consider sporotrichosis, nocardiosis, cutaneous larva migrans, anthrax (occupational in certain rural settings).

History Element	Key Questions	Diagnostic Significance
Onset	When did it start? Sudden or gradual?	Acute vs chronic aetiology
Morphology	What did it look like when it started? Has it changed?	Primary vs secondary lesion identification
Distribution	Where did it start? Where has it spread?	Pattern recognition (dermatomal, flexural, generalised)
Symptoms	Itchy? Painful? Burning?	Pruritus: eczema, scabies; Pain: infection, vasculitis
Triggers	Sun? Heat? Foods? Cosmetics?	Photosensitivity, contact allergens, urticaria triggers
Medications	New medications in last 3 months? OTC? Supplements?	Drug eruption identification, DRESS syndrome
Family history	Eczema, psoriasis, skin cancer, autoimmune disease?	Atopy, psoriasis, FAMMM syndrome
Occupation	Outdoor work? Chemical exposure? Latex?	Occupational dermatitis, UV-related malignancy

Primary & Secondary Skin Lesions

Accurate identification and description of skin lesions is fundamental to dermatological diagnosis. Lesions are classified as primary (the original pathological change) and secondary (resulting from evolution, scratching, or treatment of the primary lesion). The correct identification of lesion morphology, together with distribution and patient demographics, enables a focused differential diagnosis.

Primary Lesions

Lesion	Description	Size	Common Causes
Macule	Flat, circumscribed area of altered colour; not palpable; cannot be felt on palpation	<1 cm	Freckle, café-au-lait spot, fixed drug eruption (resolved), pityriasis versicolor, vitiligo, petechiae
Patch	Flat, circumscribed area of altered colour; not palpable	>1 cm	Vitiligo, port-wine stain, eczema (resolved), mycosis fungoides (early patch stage), pityriasis alba
Papule	Raised, solid, circumscribed lesion; palpable and elevated above the skin surface	<1 cm	Wart, mole (naevus), lichen planus, acne, insect bite, basal cell carcinoma (nodular), dermatofibroma
Nodule	Deep-seated, solid, palpable lesion extending into the dermis or subcutis	>1 cm	Lipoma, epidermoid cyst, squamous cell carcinoma, erythema nodosum, rheumatoid nodule, gouty tophus, dermatofibrosarcoma protuberans
Vesicle	Small, fluid-filled, circumscribed elevation; translucent; may be clear or straw-coloured	<0.5 cm	Herpes simplex, herpes zoster, varicella, contact dermatitis (allergic), pompholyx (dyshidrotic eczema), dermatitis herpetiformis
Bulla	Large, fluid-filled, circumscribed elevation; tense or flaccid	>0.5 cm	Bullous pemphigoid (tense), pemphigus vulgaris (flaccid), bullous impetigo, burns, friction blister, SJS/TEN, porphyria cutanea tarda
Pustule	Circumscribed, pus-filled elevation; may be follicular or non-follicular; white/yellow centre	Variable	Acne vulgaris, folliculitis, impetigo, pustular psoriasis (von Zumbusch), hidradenitis suppurativa, acute generalised exanthematous pustulosis (AGEP)
Plaque	Raised, flat-topped, palpable lesion; formed by confluence of papules	>1 cm	Psoriasis, eczema (lichenified), mycosis fungoides, cutaneous T-cell lymphoma, granuloma annulare
Wheal	Transient, raised, edematous lesion resulting from dermal oedema; migratory, non-scarring	Variable	Urticaria (acute/chronic), insect bite, urticarial vasculitis (persists >24 hrs)

Secondary Lesions

Lesion	Description	Common Causes
Scale	Visible accumulation of keratinocytes (stratum corneum); dry, flaky; may be fine or coarse	Psoriasis (silvery-white), pityriasis rosea (collarette), ichthyosis, tinea, seborrhoeic dermatitis (greasy yellow), pityriasis versicolor
Crust	Dried serum, blood, or purulent exudate on the skin surface; honey-coloured (impetigo) or haemorrhagic	Impetigo (honey-coloured), eczema herpeticum, erosive pustular dermatosis of the scalp, vasculitis, excoriation
Erosion	Loss of epidermis only; heals without scarring; moist, red base	Vesicle/bulla rupture, erosion in pemphigus, eczema (excoriated), candidiasis (intertrigo)
Ulcer	Full-thickness loss of epidermis and dermis; heals with scarring; base may be granulating or necrotic	Venous leg ulcer, arterial ulcer, pressure injury, squamous cell carcinoma, pyoderma gangrenosum, cutaneous vasculitis, leishmaniasis
Fissure	Linear crack or split in the skin; extends through the epidermis into the dermis; painful	Chronic eczema (hands/feet), angular cheilitis, tinea pedis, palmoplantar psoriasis
Excoriation	Linear or punctate erosions from scratching; often self-inflicted	Atopic dermatitis, scabies, neurotic excoriation, prurigo nodularis, chronic kidney disease–associated pruritus
Lichenification	Thickened skin with accentuated skin markings (exaggerated dermatoglyphics); from chronic rubbing	Lichen simplex chronicus, chronic atopic dermatitis, lichen planus (hypertrophic variant)
Atrophy	Thinning of the epidermis and/or dermis; skin appears translucent, wrinkled, with visible vessels	Chronic topical corticosteroid use, lichen sclerosus, anetoderma, striae (stretch marks), lipodermatosclerosis

Special Descriptors

Annular — ring-shaped with central clearing (granuloma annulare, erythema migrans, tinea corporis, annular psoriasis).
Dermatomal — following a dermatome (herpes zoster); crosses the midline only rarely.
Koebner phenomenon — new lesions appearing at sites of skin trauma (psoriasis, lichen planus, vitiligo).
Auspitz sign — pinpoint bleeding on removal of scale; classically seen in psoriasis.
Nikolsky sign — lateral pressure on apparently normal skin causes epidermal separation; positive in pemphigus vulgaris, SJS/TEN, and staphylococcal scalded skin syndrome.
Darier sign — stroking a lesion causes urtication and erythema; positive in urticaria pigmentosa (mastocytosis).

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Non-healing ulcer — red flag: Any ulcer that fails to heal within 4–6 weeks despite appropriate management should be biopsied to exclude squamous cell carcinoma, basal cell carcinoma, or other malignancy. MBS item 31356 (biopsy of skin lesion) is payable if clinically indicated.

Blistering Eruptions, Pustular Lesions & Drug Reactions

Blistering eruptions represent a spectrum of disease ranging from benign self-limiting conditions to life-threatening emergencies. The clinician must rapidly determine the level of blister formation (intra-epidermal vs sub-epidermal), assess for systemic involvement, and initiate appropriate therapy. In Australia, autoimmune blistering disease accounts for a significant burden, particularly in the elderly population.

Bullous Pemphigoid

Bullous pemphigoid (BP) is the most common autoimmune blistering disease in Australia, with an incidence of approximately 4.3 per 100,000 person-years, peaking in the seventh to eighth decades of life. It is characterised by tense, sub-epidermal blisters arising on erythematous or normal-appearing skin, predominantly on the trunk and flexural surfaces. A prodromal phase of pruritus and eczematous or urticarial plaques may precede blister formation by weeks to months.

Mild

Limited Bullous Pemphigoid

<10% BSA involvement; few blisters; minimal pruritus; limited to one anatomical region; no mucosal involvement

Setting: Outpatient dermatology

Moderate

Moderate Bullous Pemphigoid

10–30% BSA; widespread blisters; moderate to severe pruritus; may involve oral mucosa

Setting: Specialist dermatology ± day treatment

Severe

Generalised Bullous Pemphigoid

>30% BSA; extensive blistering with erosions; mucosal involvement; risk of secondary infection, fluid/electrolyte imbalance

Setting: Hospital admission — dermatology ± burns unit

Investigations: Skin biopsy for histopathology (sub-epidermal blister with eosinophils), direct immunofluorescence (linear IgG and C3 at the basement membrane zone), and serology — anti-BP180 and anti-BP230 antibodies (ELISA). Indirect immunofluorescence on salt-split skin helps localise the antigen.

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Clobetasol Propionate 0.05%

Dermovate® · Topical superpotent corticosteroid

Adult dose Apply to affected areas BID for 2–4 weeks, then taper to alternate-day dosing over 6–12 months

Notes First-line for localised–moderate BP; comparable efficacy to systemic steroids with fewer systemic side effects; monitor for skin atrophy, HPA axis suppression with prolonged use

PBS status ✔ PBS General Benefit

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Prednisolone

Solone® · Generic · Systemic corticosteroid

Adult dose 0.5–1 mg/kg/day PO as initial dose; taper over 6–12 months guided by clinical response

Notes Use for moderate–severe BP; bone protection (calcium, vitamin D, bisphosphonate if risk factors); glucose monitoring in diabetics

PBS status ✔ PBS General Benefit

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Doxycycline

Doryx® · Generic · Tetracycline antibiotic / immunomodulatory

Adult dose 200 mg PO daily (may use 100 mg BD or 200 mg OD); continue for 12 months then taper

Notes First-line steroid-sparing alternative for mild–moderate BP per 2018 Cochrane evidence; anti-inflammatory mechanism; avoids steroid side effects; well-tolerated in elderly

Paediatric dose Not recommended <8 years (tooth discolouration)

PBS status ✔ PBS General Benefit

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Mycophenolate Mofetil

CellCept® · Generic · Immunosuppressant (steroid-sparing)

Adult dose 1 g PO BD initially; titrate to 1.5–2 g BD as steroid-sparing agent

Notes Second-line steroid-sparing agent; monitor FBC, LFTs, renal function; teratogenic — ensure contraception

PBS status ⚠️ PBS Authority Required

Pemphigus Vulgaris

Pemphigus vulgaris (PV) is a severe, potentially life-threatening intra-epidermal autoimmune blistering disease caused by IgG autoantibodies against desmoglein 1 and desmoglein 3 (desmosomal adhesion proteins). It typically presents with painful, flaccid blisters that rupture easily, leaving raw, erosive surfaces. The oral mucosa is involved in 50–70% of cases and may be the presenting feature. Nikolsky sign is positive — gentle lateral pressure on clinically normal skin adjacent to a blister causes epidermal detachment.

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Pemphigus vulgaris — high-mortality disease: Without treatment, PV has a mortality rate approaching 95% within 5 years due to secondary sepsis, fluid loss, and metabolic derangement. Rituximab (anti-CD20 monoclonal antibody) is now preferred as first-line therapy per the 2020 international consensus (JAMA Dermatol 2020), achieving clinical remission in >90% of patients and enabling steroid sparing.

Key investigations: Skin biopsy — suprabasilar acantholysis (tombstone pattern) on H&E; direct immunofluorescence — intercellular IgG and C3 in a "chicken-wire" pattern within the epidermis; anti-desmoglein 1 and 3 antibody levels (ELISA). Serum antibody titres correlate with disease activity.

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Rituximab

MabThera® · Anti-CD20 monoclonal antibody

Adult dose 1 g IV on Day 1 and Day 15 (lymphoma protocol); repeat cycle at 12 months; can combine with short-course oral corticosteroids (0.5 mg/kg/day) during induction

Notes Preferred first-line for moderate–severe PV; premedicate with methylprednisolone 100 mg IV, paracetamol, and antihistamine; screen for hepatitis B (HBsAg, anti-HBc); monitor immunoglobulins

PBS status 🔴 PBS Authority Required (Specialist Only)

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Prednisolone

Solone® · Generic · Systemic corticosteroid

Adult dose 1–2 mg/kg/day PO for active disease; taper to ≤10 mg/day over 3–6 months when combined with rituximab

PBS status ✔ PBS General Benefit

Dermatitis Herpetiformis

Dermatitis herpetiformis (DH) is the cutaneous manifestation of coeliac disease, affecting approximately 1 in 10,000 people in Australia, with a strong HLA-DQ2/DQ8 association. It presents with intensely pruritic, grouped papules and vesicles distributed symmetrically on the extensor surfaces — particularly the elbows, knees, buttocks, and scalp. The hallmark is extreme itch (patients often present with excoriated, crusted lesions rather than intact vesicles because of vigorous scratching).

Diagnosis: Skin biopsy from perilesional skin (not the blister itself) demonstrating granular IgA deposits at the dermal papillae on direct immunofluorescence is the gold standard. All patients with DH should be investigated for coeliac disease (anti-tissue transglutaminase antibodies, duodenal biopsy).

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Dapsone

Generic · Sulfone antibiotic / immunomodulatory

Adult dose 50–100 mg PO daily; response within 24–48 hours (dramatic itch relief); maintenance dose 50 mg daily or alternate-day

Paediatric dose 0.5–1 mg/kg/day PO

Key precautions MUST check G6PD status before commencing (risk of severe haemolytic anaemia); baseline FBC, reticulocyte count, LFTs, renal function; monitor FBC weekly for 4 weeks, then monthly for 3 months; methaemoglobinaemia common (usually mild); agranulocytosis rare but serious

PBS status ✔ PBS General Benefit

Definitive treatment: Lifelong strict gluten-free diet — this is the cornerstone management and may reduce or eliminate the need for dapsone over 1–2 years. Referral to a dietitian with expertise in coeliac disease is essential.

Pustular Lesions

Pustular skin eruptions encompass infectious and non-infectious aetiologies. Key entities in Australian practice include:

Acute generalised exanthematous pustulosis (AGEP) — drug-induced (classically antibiotics: amoxicillin, macrolides, antimalarials); widespread small sterile pustules on erythematous base; fever, neutrophilia; resolves 1–2 weeks after drug withdrawal; distinguish from pustular psoriasis.
Pustular psoriasis (von Zumbusch) — sterile pustules on widespread erythema; systemic toxicity; may be triggered by rapid corticosteroid withdrawal, infection, or pregnancy (impetigo herpetiformis); requires urgent dermatology input.
Bacterial folliculitis — superficial pustules centred on hair follicles; common in occluded/humid environments; Staphylococcus aureus (including CA-MRSA in Australian communities) and Pseudomonas aeruginosa ("hot tub folliculitis").
Hidradenitis suppurativa — chronic, painful, inflamed nodules, abscesses, and sinus tracts in axillae, groin, and inframammary folds; Hurley staging guides treatment; referral to dermatology for moderate–severe disease.

Drug Reactions — Systematic Approach

Pattern	Description	Common Drugs	Management
Morbilliform (exanthematous)	Symmetric, maculopapular, blanching; starts trunk → extremities; onset 7–14 days after drug start; most common drug eruption (95%)	Amoxicillin, sulfonamides, phenytoin, allopurinol, antiretrovirals	Stop offending drug; antihistamines for itch; resolves 7–14 days; distinguish from viral exanthem
Urticaria / Angioedema	Transient wheals ± swelling of deeper dermis/subcutis; IgE-mediated or pseudoallergic	NSAIDs, ACE inhibitors, opioids, contrast media, penicillins	Stop drug; antihistamines; adrenaline (epinephrine) if anaphylaxis; avoid future exposure
DRESS Syndrome	Drug Reaction with Eosinophilia and Systemic Symptoms; onset 2–8 weeks; fever, facial oedema, lymphadenopathy, eosinophilia, organ involvement (liver, kidney, lung, heart)	Carbamazepine, phenytoin, allopurinol, sulfasalazine, lamotrigine, dapsone, vancomycin	Stop drug immediately; systemic corticosteroids (prednisolone 0.5–1 mg/kg/day) for severe organ involvement; dermatology ± immunology referral; monitor for autoimmune sequelae (thyroiditis, diabetes); mortality 5–10%
Fixed Drug Eruption	Single or few well-demarcated, dusky erythematous patches/plaques; recurs at the same site on re-exposure; may blister; resolves leaving post-inflammatory hyperpigmentation	NSAIDs (especially piroxicam), trimethoprim-sulfamethoxazole, tetracyclines, metronidazole, paracetamol	Stop drug; topical corticosteroids; document allergy; hyperpigmentation may persist months
SJS / TEN	Stevens-Johnson syndrome (<10% BSA detachment) / Toxic Epidermal Necrolysis (≥10% BSA); painful mucosal erosions; systemic toxicity; medical emergency	Allopurinol, sulfonamides, anticonvulsants (carbamazepine, lamotrigine, phenytoin), nevirapine, NSAIDs (piroxicam)	ICU/burns unit admission; supportive care; stop all non-essential drugs; SCORTEN score for prognosis; IV immunoglobulin or ciclosporin (specialist decision); mortality 10% (SJS) to 30–50% (TEN)

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SJS/TEN — medical emergency: Any blistering drug reaction with mucosal involvement (oral, ocular, genital erosions), skin pain disproportionate to appearance, or positive Nikolsky sign requires immediate cessation of all suspect drugs, urgent dermatology referral, and consideration of transfer to a burns/plastics unit. Calculate SCORTEN within 24 hours of admission.

Nail Examination & Approach to Lump Diagnosis

Anatomy of the Nail Unit

The nail unit comprises the nail plate (hard keratin), nail matrix (germinal epithelium), nail bed (adherent tissue beneath the plate), nail fold (proximal and lateral folds of skin), lunula (white crescent at the proximal nail), hyponychium (seal at the distal free edge), and eponychium (cuticle). Understanding this anatomy is essential for correlating nail findings with specific pathologies. Normal nail growth is approximately 3 mm/month for fingernails and 1 mm/month for toenails; a complete fingernail replacement takes 6–9 months.

Systematic Nail Examination

Examine all 20 nails under good lighting. Assess the following features systematically:

Nail Finding	Description	Differential Diagnosis
Pitting	Multiple small punctate depressions on the nail plate surface; may be fine or coarse; scattered or regular pattern	Psoriasis (most common — regular, "thimble" pitting), alopecia areata (fine, geometric pitting), eczema, lichen planus, connective tissue disease
Onycholysis	Painless separation of the nail plate from the nail bed, starting distally; creates a subungual space that may appear yellow, white, or green (if colonised by Pseudomonas)	Psoriasis, fungal infection (onychomycosis), thyrotoxicosis (hyperthyroidism), trauma, contact irritants (nail solvents, detergents), drug-induced (tetracyclines, retinoids, fluorouracil)
Koilonychia	Spoon-shaped nail — concave nail plate with upturned lateral edges	Iron deficiency anaemia (most common cause in adults), haemochromatosis, Plummer-Vinson syndrome, trauma, occupational (solvent exposure), normal variant in infants
Leuconychia	White discolouration of the nail plate; may be punctate (white spots), striate (white bands), or total	Trauma (most common — "white spots"), hypoalbuminaemia (total white nails — Terry's nails in cirrhosis), zinc deficiency, heavy metal poisoning (thallium, arsenic), fungal infection, systemic illness
Nailfold Telangiectasia	Dilated capillary loops in the proximal and lateral nail folds; best visualised with ophthalmoscope or dermatoscope at 10× magnification; may be associated with cuticular haemorrhage	Dermatomyositis (dilated, tortuous loops with haemorrhage — pathognomonic), systemic sclerosis (dilated loops with dropout areas), SLE, mixed connective tissue disease, rheumatoid arthritis
Splinter Haemorrhages	Linear, red-brown longitudinal streaks in the nail bed; distal third of nail plate; non-blanching	Trauma (most common — manual labourers), infective endocarditis, vasculitis (ANCA-associated), antiphospholipid syndrome, psoriasis
Beau's Lines	Transverse grooves/ridges affecting all nails simultaneously; indicate synchronous arrest of nail matrix growth	Systemic illness (sepsis, MI, major surgery, COVID-19), severe infection, chemotherapy, zinc deficiency, Raynaud phenomenon, Kawasaki disease (in children)
Nail Clubbing	Increased nail fold angle (>180°), loss of the normal Lovibond angle (should be <165°), "drumstick" appearance, fluctuation of the nail bed (Schamroth's window sign obliterated)	Lung cancer (most important — hypertrophic pulmonary osteoarthropathy), bronchiectasis, cystic fibrosis, interstitial pulmonary fibrosis, cyanotic congenital heart disease, inflammatory bowel disease, hepatic cirrhosis, infective endocarditis
Muehrcke's Lines	Paired, transverse, white bands separated by normal-coloured nail; non-migratory (do not grow out); seen in the nail bed	Hypoalbuminaemia (albumin <22 g/L), nephrotic syndrome, liver disease, chemotherapy, malnutrition

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Nailfold capillaroscopy: Nailfold telangiectasia with capillary dropout and giant capillary loops is a highly specific finding for systemic sclerosis. Any patient presenting with Raynaud phenomenon and nailfold changes should be investigated for connective tissue disease (ANA, anti-centromere, anti-Scl-70, ENA panel) and referred to rheumatology.

Approach to Lump Diagnosis

Lumps and swellings are among the most common presenting complaints in Australian general practice. A systematic clinical approach is essential to differentiate benign pathology (lipoma, epidermoid cyst, dermatofibroma) from potentially malignant or serious conditions (sarcoma, lymphoma, hernia).

1

History

Duration, rate of growth, pain, trauma history, systemic symptoms (weight loss, night sweats, fever), personal/family history of malignancy or connective tissue disease.

2

Inspect

Site, size (measure in cm), shape (regular/irregular), colour, surface changes (ulceration, telangiectasia), overlying skin (mobile over lump vs fixed), visible pulsation.

3

Palpate

Consistency (soft/firm/hard/fluctuant), tenderness, temperature (warm = inflammation), mobility (superficial vs deep; fixed to skin vs deep structures), edge (well-defined vs ill-defined), compressibility, reducibility (hernia), pulsatility.

4

Special Tests

Transillumination — shine a penlight through the lump; fluid-filled lesions (cyst, hydrocele) transmit light (glow); solid lesions do not. Valsalva/cough impulse — for hernias. Aspiration — diagnostic/therapeutic for suspected abscess or cyst.

5

Regional Examination

Assess draining lymph nodes (e.g., axillary nodes for upper limb lumps, inguinal nodes for lower limb). Assess neurovascular status distal to the lump. Examine for other lumps (multifocal disease).

6

Investigate & Decide

USS for superficial lumps of uncertain nature; MRI for deep soft tissue masses; FNA/core biopsy for solid or concerning lesions. Refer urgently if malignancy suspected — MBS items for USS guidance and biopsy apply.

Common Lumps — Clinical Features

Lump	Typical Features	Management
Lipoma	Soft, mobile, non-tender, well-defined, subcutaneous; slow-growing; "doughy" feel; most common on trunk, shoulders, proximal limbs	Reassurance if typical; excise if symptomatic, growing rapidly, or diagnostic uncertainty (liposarcoma if >5 cm, deep, or painful); USS confirms diagnosis
Epidermoid (sebaceous) Cyst	Firm, mobile, subcutaneous; central punctum (comedone); may discharge keratinous ("cheesy") material; common on face, trunk, scrotum	Often no treatment needed; excise if recurrent infection or bothersome; do NOT squeeze (risk of infection and incomplete removal); if infected — incise and drain + antibiotics (flucloxacillin 500 mg PO QID for 7 days)
Dermatofibroma	Firm, small (0.5–1 cm), intradermal; "dimple sign" positive (pinching causes central dimpling); brown/grey; usually on lower legs; post-insect bite or trauma	Benign; no treatment required; reassure; excise only if diagnostic doubt
Ganglion	Firm, smooth, rounded, fluctuant; transilluminates; attached to tendon sheath; most common at dorsum of wrist, also fingers (mucous cyst at DIPJ)	Reassurance (50% resolve spontaneously); aspiration (high recurrence); surgical excision if symptomatic/recurrent; avoid "Bible therapy" (striking with a book — historical practice, not recommended)
Lymph Node	Oval, firm, mobile, tender (reactive) or non-tender, matted, hard (malignant); within lymph node basins; assess for regional infection vs malignancy	Reactive: treat underlying infection; monitor for resolution over 4–6 weeks. Persistent (>6 weeks), hard, non-tender, fixed, >2 cm, or with constitutional symptoms — urgent FNA biopsy and FBC, LDH, ESR; consider lymphoma, metastatic malignancy
BCC / SCC (skin cancers)	BCC: pearly papule with telangiectasia, rolled edge, central ulceration; SCC: hyperkeratotic, ulcerated nodule, indurated; actinic keratoses are precursor lesions for SCC	Excision with appropriate margins (BCC: 3–4 mm; SCC: 4–6 mm); histopathology essential; Mohs surgery for facial BCC; refer to dermatology/plastics for high-risk features (size, site, recurrence, immunosuppression)

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Red-flag features for soft tissue lumps — urgent referral: Size >5 cm, rapid growth (>50% in 1 month), deep-seated (beneath fascia), painful without antecedent trauma, firm/hard consistency, fixed to underlying structures, associated neurovascular compromise, or constitutional symptoms. Soft tissue sarcomas are rare but carry significant morbidity and mortality — maintain a high index of suspicion. MBS item 55800 for specialist ultrasound-guided biopsy.

Special Populations

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Pregnancy

Specific dermatoses of pregnancy — atopic eruption of pregnancy (most common), polymorphic eruption of pregnancy (pruritic urticarial papules and plaques of pregnancy — PUPPP, usually third trimester), pemphigoid gestationis (bullous, anti-BP180), intrahepatic cholestasis of pregnancy (palmar itch, raised bile acids — risk of fetal distress).

Dapsone is classified as pregnancy category B2 (AU); use only if benefits outweigh risks. Avoid methotrexate (teratogenic — Category X), ciclosporin (avoid if possible), and mycophenolate (teratogenic).

Rituximab — avoid conception for 12 months after last dose; teratogenic in animal models; limited human data.

Prednisolone — pregnancy category A; considered safe at low–moderate doses; cross placenta minimally at doses <20 mg/day.

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Paediatrics

Atopic dermatitis affects ~20% of Australian children; emollient therapy is the cornerstone; topical corticosteroids (mild–moderate potency) are first-line for flares; avoid superpotent topical steroids on the face and skin folds in children.

Infantile haemangiomas — most common vascular tumour of infancy; propranolol (PBS Authority Required) is first-line treatment for complicated or functionally threatening haemangiomas; refer to paediatric dermatology/vascular anomalies clinic.

Doxycycline is contraindicated in children <8 years (dental staining, enamel hypoplasia) — use as second-line only when no alternative for BP in adolescents >8 years.

Dapsone — paediatric dose 0.5–1 mg/kg/day PO for DH; check G6PD in all children before commencing.

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Elderly

Bullous pemphigoid peaks in the 7th–8th decade; always consider BP in any elderly patient with new-onset blistering or persistent pruritic eruption.

Skin atrophy, thinning, and impaired barrier function increase susceptibility to tears, ulceration, and contact dermatitis; use lowest effective potency of topical corticosteroids.

Polypharmacy increases risk of drug eruptions — maintain a high index of suspicion for DRESS and SJS/TEN with new medications; age-related changes in drug metabolism affect clearance of dapsone and immunosuppressants.

Herpes zoster (shingles) is common and may present atypically with severe pain preceding rash by 48–72 hours; post-herpetic neuralgia risk increases with age; Shingrix® vaccine (PBS-funded for ≥65 years from November 2023).

Prednisolone in elderly — bone protection (cholecalciferol 1000 IU/day + calcium 500 mg BD; consider alendronate 70 mg PO weekly if high fracture risk); monitor blood glucose; lowest effective dose for shortest duration.

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Renal Impairment

Chronic kidney disease (CKD) causes pruritus (uraemic pruritus), acquired perforating dermatosis, calciphylaxis (painful, necrotic skin lesions — high mortality, urgent nephrology referral), and nephrogenic systemic fibrosis (if gadolinium-based contrast used in severe CKD).

Dapsone — no dose adjustment required for mild–moderate CKD; caution in severe CKD (dialysis); monitor haemoglobin closely.

Mycophenolate mofetil — avoid if eGFR <25 mL/min; if used, do not exceed 1 g BD and monitor closely.

Prednisolone — no dose adjustment but enhanced side effects in CKD (fluid retention, hypertension, glucose dysregulation).

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Hepatic Impairment

Cholestatic liver disease causes pruritus (often severe, generalised, worse at night); colestyramine (4 g PO before meals) is first-line. Spider naevi, palmar erythema, jaundice, and Terry's nails are dermatological stigmata of chronic liver disease.

Dapsone is hepatically metabolised — use with caution in significant hepatic impairment; monitor LFTs; dose reduction may be necessary.

Methotrexate is contraindicated in significant hepatic impairment (Child–Pugh B or C).

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Immunocompromised

Patients on rituximab are at increased risk of hepatitis B reactivation — screen all patients (HBsAg, anti-HBs, anti-HBc) prior to initiation; entecavir prophylaxis for HBV-positive patients.

Rituximab-associated hypogammaglobulinaemia — monitor immunoglobulin levels (IgG) every 3–6 months; IV immunoglobulin replacement if IgG <4 g/L with recurrent infections.

HIV-positive patients — atypical presentations of common dermatoses; high prevalence of psoriasis (severe), seborrhoeic dermatitis, oral hairy leukoplakia, Kaposi sarcoma (HHV-8), molluscum contagiosum, and drug eruptions (especially to nevirapine and trimethoprim-sulfamethoxazole).

Organ transplant recipients — 65–250× increased risk of SCC; rigorous skin cancer surveillance every 6–12 months; consider reducing immunosuppression in consultation with transplant team for recurrent/multiple skin cancers.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Skin conditions are disproportionately prevalent in Aboriginal and Torres Strait Islander communities, particularly in remote and very remote areas of northern and central Australia. The Healthy Skin Program in the Northern Territory, operating since 2004, has demonstrated that community-based interventions can significantly reduce scabies and impetigo prevalence. However, skin infections remain a major public health concern, with implications for rheumatic heart disease (RHD) prevention and chronic kidney disease.

Scabies and Skin Infection Burden

Scabies prevalence in remote Aboriginal communities ranges from 30–70% in children <2 years, compared to <5% in the general Australian population. Scabies leads to secondary bacterial infection (impetigo) with group A Streptococcus (GAS) and Staphylococcus aureus (including CA-MRSA), which drives post-streptococcal glomerulonephritis and acute rheumatic fever (ARF). The RHDAustralia CARPA Manual recommends mass drug administration (MDA) with ivermectin (200 μg/kg PO, Day 1 and Day 14) or permethrin 5% cream for scabies control in communities.

Rheumatic Heart Disease Prevention

Aboriginal and Torres Strait Islander Australians have among the highest rates of ARF and RHD globally. Skin sores (impetigo/pyoderma) are a major portal of entry for GAS infection. Effective skin infection management is a cornerstone of RHD prevention — early treatment of impetigo with oral antibiotics (e.g., cephalexin or clindamycin) and topical antiseptic measures (daily washing with soap and water, application of white petrolatum) reduces GAS transmission.

Access to Dermatology Services

Specialist dermatology services are extremely limited in remote Australia; most communities rely on visiting specialists, remote health practitioners, and store-and-forward teledermatology. The Australian Government funds Aboriginal Community Controlled Health Organisations (ACCHOs) to deliver primary care, but skin-specific programs often lack sustainable funding. Teledermatology platforms (e.g., NT Department of Health Skin Tracker) enable remote specialist review with clinical photographs.

Cultural Considerations

Skin conditions carry significant cultural and social stigma in some Aboriginal communities. Gender considerations are important — male health workers may need to be involved in the examination of male patients in some communities, and kinship relationships may affect the acceptability of healthcare provision. Yarning about skin health in a culturally safe environment improves engagement. Appropriate use of interpreters when English is a second or third language is essential.

Environmental and Housing Factors

Overcrowded housing, limited access to running water, and environmental conditions (heat, humidity) in remote communities contribute to high rates of skin infection. Effective skin disease management requires a holistic, "Healthy Skin" approach encompassing individual treatment, household treatment, community education, and advocacy for improved housing, water supply, and hygiene infrastructure.

Skin Cancer Patterns

While melanoma rates are lower in Aboriginal and Torres Strait Islander Australians compared to non-Indigenous Australians (due to higher melanin in skin), skin cancers that do occur are often diagnosed at later stages, particularly in remote areas with limited access to screening. BCC and SCC still occur and should not be overlooked. Culturally appropriate skin cancer awareness programs are needed.

📚 References

1. Australian Institute of Health and Welfare (AIHW). Skin cancer in Australia. Cat. no. CAN 172. Canberra: AIHW; 2024.
2. Venning VA, Taghipour K, Mohd Mustapa MF, et al. British Association of Dermatologists' guidelines for the management of bullous pemphigoid 2012. Br J Dermatol. 2012;167(6):1200–1214.
3. Joly P, Maho-Vaillant M, Prost-Squarcioni C, et al. First-line rituximab combined with short-term prednisone versus prednisone alone for the treatment of pemphigus (Ritux 3): a prospective, multicentre, parallel-group, open-label randomised trial. Lancet. 2017;389(10083):2031–2040.
4. Murrell DF, Peña S, Joly P, et al. Diagnosis and management of pemphigus: recommendations of an international panel of experts. J Am Acad Dermatol. 2020;82(3):575–585.
5. Reunala T, Salmi TT, Hervonen K, et al. Dermatitis herpetiformis: a common extraintestinal manifestation of coeliac disease. Nutrients. 2018;10(5):602.
6. Australasian College of Dermatologists (ACD). Guidelines for the management of psoriasis in Australia. Sydney: ACD; 2022.
7. Bowen AC, Mahé A, Hay RJ, et al. The global epidemiology of impetigo: a systematic review of the population prevalence of impetigo and pyoderma. PLoS One. 2015;10(8):e0136789.
8. RHDAustralia (RHD Australia), a program of Menzies School of Health Research. The 2020 Australian guideline for prevention, diagnosis and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: RHDAustralia; 2020.
9. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th ed. (Red Book). Melbourne: RACGP; 2016 (updated 2018).
10. Ngan V, Oakley A, Rademaker M. DermNet NZ — The dermatology resource. Hamilton, NZ: DermNet Trust; 2024. Available at: dermnetnz.org.
11. Andrews' Diseases of the Skin: Clinical Dermatology. James WD, Elston DM, Treat JR, Rosenbach MA, Neuhaus IM, eds. 13th ed. Philadelphia: Elsevier; 2020.
12. Danby SG, Cork MJ. New concepts in skin barrier function and therapy. Curr Opin Allergy Clin Immunol. 2020;20(5):448–455.
13. Roberts LJ, Huffam SE, Walton SF, Currie BJ. Crusted scabies: clinical and immunological findings in seventy-eight patients and a review of the literature. J Infect. 2006;52(5):375–381.
14. Duarte AF, Correia O, Barros AM, Azevedo F, Haneke E. Nail psoriasis: an unsolved problem. J Eur Acad Dermatol Venereol. 2020;34(5):965–974.
15. Salvarani C, Pipitone N, Versari A, Hunder GG. Clinical features of polymyalgia rheumatica and giant cell arteritis. Nat Rev Rheumatol. 2012;8(9):509–521. [Re: nailfold capillaroscopy and connective tissue disease assessment.]