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Dermatology

Rashes, lesions and describing what you see.

Use as a study guide only. These notes are part of a free open-access medical education (FOAMed) project and may contain errors or outdated information. Always verify against current guidelines (e.g. eTG, RACGP, local health district policies) and reputable sources before applying anything to patient care. See the full disclaimer.

From the wards

Clinical pearls & learnings

Tips and tricks collected over the years — a living list that grows with every rotation. Use as a study guide only and check current guidelines before acting on anything.

Ulcers, cysts & pitted lesions

The painless foot ulcer — three to consider
CauseKey features
Venous ulcerGaiter area (medial malleolus), irregular/shallow, associated oedema, hemosiderin staining and varicosities
Buruli ulcer (Mycobacterium ulcerans)Endemic to parts of coastal Victoria and northern Australia; starts as a painless nodule that breaks down into an ulcer with undermined edges — painless because the toxin (mycolactone) suppresses local immune response and damages nerves
Neuropathic ulcer (T2DM)Over pressure points (plantar surface, metatarsal heads); painless due to loss of protective sensation from peripheral neuropathy
Pitted keratolysis

A bacterial infection (Kytococcus sedentarius and related species) causing malodorous, punched-out pits on the sole, associated with hyperhidrosis and occlusive footwear. Treat with a topical antibiotic — mupirocin, clindamycin or fusidic acid — alongside moisture control (antiperspirants, breathable footwear, moisture-wicking socks).

Dermoid cyst

A dermoid cyst is a mature (benign) teratoma — a congenital cyst containing tissue from multiple germ layers (skin appendages, hair, sebaceous material, occasionally teeth or cartilage), typically found along embryonic fusion lines such as the lateral eyebrow, midline nose, or scalp.

Skin infections

Angular cheilitis

Often polymicrobial: Candida albicans (isolated in around 93% of cases) and Staphylococcus aureus (around 20%) frequently coexist, alongside Streptococcus species.

  • Risk factors: type 2 diabetes, immunocompromise, older age, ill-fitting dentures, nutritional deficiency (iron, B12, folate, riboflavin), and a lip-licking/drooling habit that keeps the skin folds chronically moist.
Molluscum contagiosum

Dome-shaped, umbilicated papules with a pearly, rounded edge — classically across the trunk. Spread is by direct skin contact (including sexual contact in adults); in children, genital lesions are usually from autoinoculation/spread from other body sites rather than a marker of abuse, though the possibility should still be considered appropriately in context.

Self-limiting in immunocompetent patients — most resolve within 6–18 months without treatment, so deroofing/curettage isn't routinely needed. Active treatment is reserved for persistent, cosmetically bothersome, or immunocompromised cases.

Erythrasma

Corynebacterium minutissimum infection causing well-demarcated red-brown patches in skin folds (groin, axillae, toe webs) — fluoresces coral-pink under Wood's lamp (coproporphyrin III), a quick bedside way to distinguish it from tinea.

Treatment: topical fusidic acid first-line, oral or topical erythromycin second-line (or for more widespread disease).

Non-bullous impetigo

Choosing therapy

ScenarioTreatment
1–3 lesions, not in a high-risk groupTopical mupirocin ointment
Aboriginal and Torres Strait Islander or remote communitiesOral flucloxacillin preferred — higher burden of streptococcal disease and downstream complications (post-streptococcal glomerulonephritis, rheumatic fever)
Penicillin allergyOral cefalexin for a mild/non-severe allergy — use a non-beta-lactam alternative (e.g. trimethoprim-sulfamethoxazole, clindamycin) if the allergy history is severe/anaphylactic
Dissecting cellulitis of the scalp

Also called perifolliculitis capitis abscedens et suffodiens — part of the follicular occlusion tetrad alongside hidradenitis suppurativa, acne conglobata and pilonidal disease. Painful nodules with interconnecting sinus tracts and purulent discharge.

  • Oral doxycycline (± rifampicin) for milder disease.
  • Intralesional corticosteroid injections for inflammatory nodules.
  • Oral isotretinoin where there's scarring, keloid formation or patchy alopecia.
  • Biologics (e.g. adalimumab) are an emerging option for refractory disease.

Inflammatory & genital dermatoses

Perioral dermatitis

Remove the trigger — classically topical corticosteroid use (even low-potency), and heavy/occlusive moisturisers or cosmetics — plus oral doxycycline for 6–12 weeks. Expect an initial flare after stopping steroids before it improves; topical metronidazole or erythromycin can be used for milder disease.

Lichen sclerosus (genital)

In males, the genital form is also called balanitis xerotica obliterans (BXO) — white, atrophic patches causing a tight foreskin that can't be fully retracted (phimosis), which can progress to urethral meatal stenosis and a deviated or spraying urinary stream. Circumcision is often required where phimosis is significant.

In females, lichen sclerosus classically causes itchy, atrophic white plaques in a "figure-of-8" distribution around the vulva and perianal skin, with a small increased long-term risk of vulval squamous cell carcinoma — worth long-term follow-up.

Guttate psoriasis

Small, "drop-like" papules over the trunk and proximal limbs, classically triggered by a preceding infection — usually streptococcal (e.g. tonsillitis). May resolve spontaneously over weeks to months, though a subset go on to develop chronic plaque psoriasis.

Vascular & bullous conditions

Infantile haemangioma (strawberry naevus)

Usually absent or minimal at birth, appearing in the first few weeks of life, then growing rapidly through the first year (proliferative phase) before spontaneously regressing over the following years (involution) — this growth-then-regression pattern is what distinguishes it from a vascular malformation, which is present at birth and grows proportionately with the child without regressing.

Most need no treatment. Oral propranolol is first-line where treatment is indicated — ulceration, visual axis or airway compromise, or a cosmetically significant facial lesion.

Stevens-Johnson syndrome / toxic epidermal necrolysis (SJS/TEN)

Classified by body surface area with epidermal detachment

EntityBSA detached
SJS<10%
SJS/TEN overlap10–30%
TEN>30%

Classic culprits: allopurinol, anticonvulsants (carbamazepine, lamotrigine, phenytoin), sulfonamides, and NSAIDs.

Stop the culprit drug immediately and manage as a medical emergency — patients need burns unit/ICU-level supportive care given the risk of sepsis, fluid loss and multi-organ involvement.

Bullous pemphigoid

An autoimmune subepidermal blistering disease — typically older patients, intensely itchy, tense bullae on an erythematous/urticated base, mainly the trunk and proximal limbs. Mucous membranes are usually spared, and the bullae are tense (unlike pemphigus vulgaris, which more often involves mucosa and has flaccid, easily ruptured blisters) — a useful bedside differentiator.

Paediatric fever & rash

Erythema toxicum neonatorum

A benign, self-limiting neonatal rash requiring no treatment beyond parental reassurance — typically appears within the first few days of life and resolves spontaneously within 1–2 weeks.

Fever + rash — sorting the differential
ConditionRash timing vs feverDistributionClassic appearanceKey distinguishing features
Measles3–4 days after fever onsetHead/face → spreads downwardErythematous maculopapularChild remains unwell; Koplik spots
Roseola infantum (HHV-6/7)After 3–5 days of fever, as fever resolvesTrunk first, then neck & proximal limbsFine pink macules/papulesWell child when rash appears
RubellaSame time or shortly after feverFace → trunk → extremitiesFine maculopapularLymphadenopathy (post-auricular/suboccipital), mild illness
Parvovirus B19After systemic symptoms resolveCheeks → arms & legs"Slapped cheek", then lacy reticular rashNasal ridge & perioral sparing; no longer infectious once rash appears
EnterovirusLate in illnessVariableNon-specific maculopapularOften mild viral features
Scarlet fever (GAS)12–48h after fever onsetGeneralised, trunk predominantFine sandpaper-like rashStrawberry tongue, circumoral pallor, Pastia's lines in skin folds
Hand, foot and mouth diseaseWith or shortly after fever onsetMouth, palms, soles, buttocksGrey elliptical vesiclesOral ulcers common
Varicella (primary — chickenpox)24–48h after prodromeTrunk & face first → peripheryPapules, vesicles, pustules & crusts togetherLesions in multiple stages at once ("crops")
Varicella (secondary — shingles)± feverDermatomal, unilateralClusters of vesicles on erythematous baseVZV reactivation
Kawasaki diseaseDuring febrile phase (≥5 days fever)Polymorphous, often trunk/perineumPolymorphous, non-vesicular rashMucocutaneous changes — conjunctivitis, red/cracked lips, strawberry tongue, extremity changes, cervical lymphadenopathy
MeningococcaemiaWithin hours of fever onsetTrunk & limbsPetechial or purpuric, non-blanchingToxic-appearing child — medical emergency
Gianotti-Crosti syndromeVariable, post-viralExtensor limbs, buttocks, face; trunk sparedPapular or papulovesicularSymmetrical eruption, child often well

Two diagnoses on this list must never be missed. Kawasaki disease untreated carries a real risk of coronary artery aneurysm — treat (IVIG + aspirin) on clinical grounds without waiting for a confirmatory test. Meningococcaemia with a non-blanching rash and fever is a medical emergency — same-day assessment and IV antibiotics without delay.