Rapid review: dermatology

• This page is a revision shortcut through dermatology: each block gives the picture in plain clinical words, the most likely diagnosis, the best first test, the best first treatment, the trap, and a pointer to the full MedGrasp topic.
• Pattern recognition does most of the work. The discriminating feature is usually simple: where is the rash, is it itchy or painful, is the blister flaccid or tense, is the lesion change asymmetric, and is the patient otherwise well.
• Rashes and infections are usually clinical diagnoses. Swabs, patch tests, biopsies and cultures are used to confirm, not to replace examining the whole patient.
• A red flag always wins over a favourite diagnosis: pain out of proportion, rapidly spreading erythema, mucosal erosions, airway swelling, immunosuppression, or a changing pigmented lesion.
• Many skin treatments are topical. Emollients are the backbone of eczema; topical corticosteroids come in potencies that must be matched to age, site and severity.
• Low-resource and high-resource messages are the same: look carefully, measure the redness rather than guessing, stop the offending drug in any severe reaction, and escalate early when tissue is at risk.

By the end of this page you should be able to:

1. Recognise the classic presentations of the common skin diseases listed in this review.
2. State the single most likely diagnosis and the best first test for each presentation.
3. Choose the first, evidence-based treatment, including the first drug, its route and duration where the sources specify it.
4. List the most common wrong answer that slows an exam answer or a clinical decision.
5. Separate benign from malignant pigmented lesions and state the excision margins used in skin cancer.
6. Recognise Stevens-Johnson syndrome or toxic epidermal necrolysis and necrotising fasciitis as emergencies and outline their immediate management.
7. Use the flowchart in this page to structure the approach to a red rash or a red swelling.
8. Link from every block to the full MedGrasp topic that explains the reasoning.

Each section follows the same five lines, so you can scan a whole area in seconds. The first line is the picture as the patient or the examiner describes it. The last line is the trap: the answer that looks reasonable but is usually wrong, or the diagnosis you reach when you stop thinking too early. Numbers are taken from the guideline named in that block. Behaviour and disease vary by setting, so use your local formulary before prescribing.

Presenting picture. A recurring itchy rash, worse at night, with dry, sensitive skin; in infants the cheeks and extensor surfaces are involved, in children and adults the flexures, neck and wrists. There may be a family history of atopy and triggers such as soaps, cold air and stress.

Most likely diagnosis. Atopic dermatitis (eczema). The diagnosis is clinical. Consider allergic contact dermatitis when the rash maps to a product, seborrhoeic dermatitis in infants and on the scalp, psoriasis when the plaques are well-demarcated and on extensors, and fungal infection when the rash is annular with a scaly edge.

Best first test. Apply the NICE under-12 criteria: an itchy skin condition plus at least 3 of the listed features. ^[1] No blood test is needed in a typical case. Test for allergy when the history suggests it, and use patch testing before labelling chronic, poorly responding eczema in an adult as "atopic".

Best first treatment. Emollients are the basis of management and should always be used, even when the skin is clear. ^[1] Prescribe leave-on emollients in large quantities, 250 g to 500 g weekly. ^[1] Topical corticosteroids are first-line for flares, applied once or twice daily, and treatment should continue for about 48 hours after the symptoms settle. ^[1] Match potency to age, site and severity: short-term (3 to 5 days) moderate potency for severe flares, 7 to 14 days for potent or very potent preparations in the axillae or groin, potent preparations for no more than 14 days and not on the face or neck, and potent preparations in children from 12 months for as short a time as possible. ^[1] For the face and neck, calcineurin inhibitors remain the preferred option. ^[1] For frequent flares, 2 or 3 a month, a topical corticosteroid on 2 consecutive days each week for 3 to 6 months is a useful strategy. ^[1] Do not offer emollient bath additives. ^[1] Calcineurin inhibitors are second-line for moderate disease, including the face and neck in children aged 2 years or more. ^{[1] [12] [6]}

Commonest wrong answer. Prescribing antihistamines as the main treatment and skimping on emollient; stopping the steroid as soon as itch stops; using a single potency for every site and age; blaming diet without evidence. Antihistamines are only useful against itch, and emollients are the therapy, not a cosmetic extra.

Full topic: Atopic dermatitis (dermatology/atopic-dermatitis).

Presenting picture. Irritant or allergic contact dermatitis is a rash with a sharp outline that matches the site of contact, often vesicular when acute. Seborrhoeic dermatitis favours the scalp, eyebrows, nasolabial folds and chest. Stasis dermatitis affects the lower legs in the setting of venous disease.

Most likely diagnosis. Contact dermatitis in a patient with a relevant exposure; seborrhoeic dermatitis in the scalp and folds; stasis dermatitis when there is oedema, haemosiderin staining and ulceration.

Best first test. History of exposure and, where allergy is suspected, patch testing. In stasis dermatitis, assess the venous system and exclude cellulitis and thrombosis.

Best first treatment. Remove the cause when possible; short courses of topical corticosteroids; calcineurin inhibitors for facial and flexural disease; for stasis dermatitis, compression therapy and skin care, with referral for venous intervention where indicated.

Commonest wrong answer. Calling all lower-leg rashes "cellulitis"; missing venous disease; or treating seborrhoeic dermatitis only with antifungal cream without addressing sebum and scale.

Full topic: Contact, seborrhoeic and stasis dermatitis (dermatology/contact-seborrhoeic-and-stasis-dermatitis).

Presenting picture. Erythematous, well-demarcated plaques with silvery scale on the extensor surfaces, scalp and sacrum; nail pitting or onycholysis; a recent sore throat before a guttate eruption.

Most likely diagnosis. Plaque psoriasis, guttate psoriasis in younger patients, pustular or erythrodermic variants. Distinguish from atopic dermatitis, which is more flexural and pruritic, and from tinea, which is usually asymmetric and annular.

Best first test. Clinical grading with PASI and BSA. How many people with psoriasis develop psoriatic arthritis is not quantified in NICE CG153; estimates from other sources range widely (from about one in five to about one in three), and the National Psoriasis Foundation puts the figure at roughly one in three. ^[19] An annual joint screen is needed regardless, especially in the first 10 years. ^[2] Cardiovascular risk should be assessed in severe disease.

Best first treatment. Topical treatment is first-line. ^[2] For trunk and limb disease in adults, offer a potent corticosteroid once daily plus vitamin D or a vitamin D analogue once daily (separately, one in the morning and the other in the evening) for up to 4 weeks, and aim for a break of 4 weeks between courses of potent or very potent corticosteroids. ^[2] If this does not clear the plaque, use a vitamin D analogue twice daily for 8 to 12 weeks. ^[2] For scalp psoriasis, offer a potent corticosteroid once daily for up to 4 weeks. ^[2] Moderate to severe disease needs phototherapy, conventional systemics led by methotrexate, then biologics. ^[1]

Commonest wrong answer. Treating psoriasis indefinitely with a potent steroid without a break; using a mild steroid on thick plaques and being surprised when it fails; missing psoriatic arthritis or the cardiovascular risk.

Full topic: Psoriasis (dermatology/psoriasis).

Presenting picture. Itchy wheals and oedema that appear and disappear within 24 hours, with no scale and normal skin between, sometimes with lip or eyelid swelling. Acute means under 6 weeks; chronic means wheals on most days for more than 6 weeks. ^[3]

Most likely diagnosis. Acute urticaria after infection, drugs or allergen in most, chronic spontaneous urticaria beyond 6 weeks. Chronic urticaria is defined by time, not by a single cause, and is not usually an allergy.

Best first test. Clinical diagnosis. In chronic spontaneous urticaria, tests such as full blood count, ESR, CRP and thyroid function screens for an obvious trigger; chronic inducible urticaria needs the specific provocation test.

Best first treatment. A standard dose of a second-generation H1 antihistamine. ^[3] Increase up to four times the standard dose if the response is incomplete, then refer for omalizumab and, if needed, ciclosporin. ^[3] About 40% of chronic spontaneous urticaria patients are controlled with up to four times the standard antihistamine dose, and the response can rise to about 70% once omalizumab is added. ^[3] Acute episodes usually need only a standard-dose antihistamine and reassurance.

Commonest wrong answer. Reaching for first-generation, sedating antihistamines; giving systemic corticosteroids for a benign self-limiting rash; attributing all chronic urticaria to food or allergy without evidence.

Full topic: Urticaria, angioedema and hypersensitivity (dermatology/urticaria-and-hypersensitivity-reactions).

Presenting picture. A new, usually morbilliform, itchy rash beginning one to two weeks after starting a medicine, often settling within days of stopping it. The skin looks widespread and symmetric; systemic features may be minimal.

Most likely diagnosis. A benign exanthematous drug eruption. The skill is to stop at every new rash and ask whether it is an early severe cutaneous adverse reaction.

Best first test. Clinical, with a careful drug and timing history. Drug-induced cutaneous reactions most often appear after a new prescription. ^[17] Tests are used to exclude mimics and to grade severity rather than to prove causation.

Best first treatment. Stop the suspected drug and give antihistamines and emollients; most mild eruptions recover. Do not restart the suspected drug. Urgent multidisciplinary care is required when there is fever, eosinophilia, mucosal erosions, blistering or epidermal detachment.

Commonest wrong answer. Reassuring a patient that a rash is "just a viral rash" without reviewing the medication list, or prescribing antibiotics for a morbilliform drug eruption. The real traps are missing DRESS, Stevens-Johnson syndrome or toxic epidermal necrolysis by assuming the rash is benign.

Full topic: Drug eruptions, erythema multiforme and SJS/TEN (dermatology/drug-eruptions-and-severe-cutaneous-reactions).

Presenting picture. Highly contagious superficial sores with golden-brown crusts (non-bullous impetigo) or large flaccid blisters (bullous impetigo), usually on the face or limbs in children.

Most likely diagnosis. Impetigo, usually staphylococcal or streptococcal. Bullous impetigo is toxigenic Staphylococcus aureus.

Best first test. Clinical. Consider a swab for culture and resistance, including methicillin-resistant S. aureus, in recurrent or treatment-resistant cases.

Best first treatment. NICE guidance: for localised non-bullous impetigo, apply hydrogen peroxide 1% cream two or three times a day for 5 days, or fusidic acid 2% three times a day for 5 days when hydrogen peroxide is unsuitable or ineffective. ^[6] For oral therapy, flucloxacillin for adults is 500 mg four times a day for 5 days, or clarithromycin 250 mg twice a day for 5 days (increased to 500 mg twice a day for severe infection) if penicillin-allergic. ^[6] Return to school or work after 48 hours of effective treatment.

Commonest wrong answer. Using a single topical antibiotic repeatedly and creating resistance, or prescribing oral antibiotics when a simple crust can be treated topically. For more than a few lesions, or for bullous disease, systemic treatment is appropriate.

Full topic: Impetigo, cellulitis and necrotising fasciitis (dermatology/bacterial-skin-infections-impetigo-cellulitis-necrotising).

Presenting picture. A hot, red, swollen, tender area spreading over hours to days, often on a leg; distinct sharp raised edge in erysipelas. There may be fever, tachycardia and lymphangitis.

Most likely diagnosis. Cellulitis or erysipelas, usually streptococcal or staphylococcal. The main mimics are deep vein thrombosis, gout, stasis dermatitis, contact dermatitis and (rarely) necrotising fasciitis.

Best first test. Clinical. Swab any portal of entry, and take blood cultures only in severe, hospitalised disease. Consider Doppler ultrasound if thrombosis is realistic.

Best first treatment. NICE NG141 recommends flucloxacillin 500 mg to 1 g four times a day by mouth for 5 to 7 days, or 1 g to 2 g four times a day intravenously when the patient is unwell or unable to take oral medication; clarithromycin 500 mg twice daily is the first alternative in penicillin allergy. ^[5] Other alternatives include doxycycline 200 mg on day one then 100 mg once daily for a 5 to 7 day total, and co-amoxiclav for facial or periorbital cellulitis or animal bites. ^[5] Start oral treatment where possible and review intravenous therapy by 48 hours. ^[5] Up to 14 days may be needed in some cases. ^[5]

Commonest wrong answer. Treating a mimic such as stasis dermatitis or gout as cellulitis for weeks; or undertreating early necrotising disease because the patient still looks well.

Full topic: Impetigo, cellulitis and necrotising fasciitis (dermatology/bacterial-skin-infections-impetigo-cellulitis-necrotising).

Presenting picture. Severe skin pain that is out of proportion to the clinical appearance, with rapidly spreading erythema, heat, oedema beyond the red area, bullae, skin colour change or sudden cutaneous anaesthesia.

Most likely diagnosis. Necrotising fasciitis, a surgical emergency. Mortality is around 20 to 30%, rising when surgery is delayed. ^[7]

Best first test. Clinical diagnosis. Imaging for gas along fascial planes supports the diagnosis, but surgery must not be delayed while waiting for CT. The LRINEC score classifies risk using C-reactive protein, leucocyte count, haemoglobin, sodium, creatinine and glucose, and may support the diagnosis, but a normal score does not exclude disease. ^[7]

Best first treatment. Resuscitate, give broad-spectrum intravenous antibiotics that cover Gram-positive, Gram-negative and anaerobic organisms, and arrange emergency surgical debridement as soon as possible; re-examine the wound every 12 to 24 hours. ^[7]

Commonest wrong answer. Waits for imaging or laboratory confirmation before operating; or assumes the low-risk LRINEC end of the score reassures. Pain out of proportion and rapid spread are the clinical triggers.

Full topic: Impetigo, cellulitis and necrotising fasciitis (dermatology/bacterial-skin-infections-impetigo-cellulitis-necrotising).

Presenting picture. Pemphigus vulgaris: painful oral erosions followed by flaccid, easily ruptured blisters on normal skin, with a positive Nikolsky sign. Bullous pemphigoid: tense, robust blisters on an itchy or urticarial base, often in older adults, with a negative Nikolsky sign.

Most likely diagnosis. Pemphigus vulgaris (intraepidermal split, anti-desmoglein antibodies) or bullous pemphigoid (subepidermal split, anti-BP180/230 antibodies). The bedside check is Nikolsky, backed by histology and direct immunofluorescence: a fishnet pattern in pemphigus and a linear band in bullous pemphigoid.

Best first test. Biopsy of the blister edge for histology and of perilesional skin for direct immunofluorescence. Pemphigus gives an intraepidermal split; bullous pemphigoid gives a subepidermal split with antibody deposition at the basement membrane.

Best first treatment. Pemphigus vulgaris: systemic corticosteroid, prednisolone at 0.5 to 1.5 mg per kg per day, plus a steroid-sparing agent such as azathioprine or mycophenolate, with rituximab at 1 g twice, 2 weeks apart, allowing faster steroid tapering. ^[9][18] Bullous pemphigoid: superpotent topical corticosteroids first; in extensive or frail disease, oral prednisolone 0.5 mg per kg per day or doxycycline 200 mg a day are first-line systemic options. ^[8]

Commonest wrong answer. Treating pemphigus as if it were bullous pemphigoid, or the reverse; forgetting that bullous pemphigoid in frail elderly patients responds to doxycycline with fewer adverse effects; or omitting steroid-sparing therapy and allowing prolonged high-dose steroid toxicity.

Full topic: Pemphigus vulgaris and bullous pemphigoid (dermatology/pemphigus-and-bullous-pemphigoid).

Presenting picture. Stable seborrhoeic keratoses are waxy, stuck-on plaques in older adults; melanocytic naevi are round, symmetric and uniform; dermatofibromas are firm nodules with a dimple sign.

Most likely diagnosis. Benign skin tumour or naevus. Change, irregularity or a lesion that looks different from a person's others is the signal to investigate further.

Best first test. Dermoscopy by a trained clinician; excision with histology when any doubt exists.

Best first treatment. Reassurance or cosmetic removal when benign; never excise a pigmented lesion without histology.

Commonest wrong answer. Diagnosing a changing pigmented lesion as a harmless naevus without histology, or removing an undifferentiated lesion by diathermy and losing the diagnosis.

Full topic: Benign skin tumours and naevi (dermatology/benign-skin-tumours-and-naevi).

Presenting picture. A pigmented lesion new or changing in asymmetry, border, colour, diameter (often above 6 mm, although melanomas can be smaller) ^[20] or evolution, or a lesion that looks unlike a person's other moles (the "ugly duckling").

Most likely diagnosis. Cutaneous melanoma until proven otherwise. It grows from melanocytes and is linked to ultraviolet exposure.

Best first test. Full-thickness excision biopsy with a small clinical margin. Do not shave or curette a suspected melanoma; histology gives Breslow thickness, the basis of staging. ^[10]

Best first treatment. Complete excision, 1 cm when the melanoma is stage I (and when a 2 cm margin would carry unacceptable morbidity) and 2 cm when it is stage II. ^[10] Thicker melanomas may need sentinel lymph node assessment by a specialist team.

Commonest wrong answer. Watching a changing lesion because it is "probably just a mole", or taking a shaving biopsy that underestimates depth. Excision with a measured margin is both diagnostic and therapeutic.

Full topic: Melanoma (dermatology/melanoma).

Presenting picture. Basal cell carcinoma is a pearly, telangiectatic nodule or plaque with a rolled edge and may ulcerate; squamous cell carcinoma is a firm scaly nodule, plaque or ulcer, often on sun-damaged skin; Merkel cell carcinoma is a rapidly growing, shiny red or violaceous nodule on sun-exposed skin in older people.

Most likely diagnosis. Basal cell carcinoma, cutaneous squamous cell carcinoma, or (rarely) Merkel cell carcinoma. Risk is driven by cumulative ultraviolet exposure, fair skin, age and immunosuppression, notably in transplant recipients.

Best first test. Clinical diagnosis with dermoscopy; biopsy of suspicious lesions and of any non-healing ulcer. NICE NG12 supports prompt recognition and referral where cancer is suspected. ^[11]

Best first treatment. Excision with an appropriate measured margin, Mohs micrographic surgery for high-risk or anatomically sensitive lesions, radiotherapy where surgery is not suitable, topical or field therapy for superficial lesions, and systemic therapy for metastatic or Merkel cell disease within specialist teams.

Commonest wrong answer. Treating an undifferentiated, slowly healing skin cancer with repeated creams without a biopsy; or assuming that basal cell carcinoma "never spreads" removes the need for treatment, even though local invasion can be destructive.

Full topic: Basal cell carcinoma, squamous cell carcinoma and Merkel (dermatology/keratinocyte-cancers-and-merkel-cell-carcinoma).

Presenting picture. Well-demarcated, chalky-white patches that are accentuated under a Wood's lamp; often symmetric on the hands, face and (in non-segmental vitiligo) flexures. In adults, melasma appears as brown patches on the cheeks, forehead and upper lip.

Most likely diagnosis. Vitiligo (non-segmental; symmetric patches) or melasma; consider post-inflammatory pigment change, pityriasis alba and tinea versicolor in the differential.

Best first test. Clinical, with Wood's lamp; check thyroid function, since thyroid disease is the most common autoimmune association.

Best first treatment. Photoprotection, potent topical corticosteroids once daily or topical calcineurin inhibitors twice daily, narrowband UVB when disease is widespread or active, and ruxolitinib cream for eligible patients aged 12 years or more with non-segmental disease. ^[12] Re-pigmentation takes months.

Commonest wrong answer. Stopping treatment too early, or dismissing vitiligo as purely cosmetic.

Full topic: Vitiligo and disorders of pigmentation (dermatology/vitiligo-and-pigment-disorders).

Presenting picture. Comedones (blackheads and whiteheads), papules, pustules and nodules centred on pilosebaceous units on the face, neck, back and chest, most often in adolescence.

Most likely diagnosis. Acne vulgaris. Distinguish acneiform eruption, rosacea (no comedones, different distribution), perioral dermatitis and folliculitis.

Best first test. Clinical grading by lesion type and count. No routine microbiology is needed.

Best first treatment. NICE advises offering a 12-week first-line course chosen by severity and preference: a fixed combination of adapalene with benzoyl peroxide, tretinoin with clindamycin, benzoyl peroxide with clindamycin, or (for moderate to severe acne) a topical combination plus oral lymecycline or doxycycline, or azelaic acid with oral lymecycline or doxycycline. ^[15] Fixed topical combinations are usually applied once daily in the evening, whereas topical azelaic acid is applied twice daily. ^[15] Refer for oral isotretinoin for severe, scarring or persistently refractory acne.

Commonest wrong answer. Prescribing an oral antibiotic alone without a topical retinoid or benzoyl peroxide; or prescribing isotretinoin without adequate preceding therapy.

Full topic: Acne vulgaris, folliculitis and pilonidal disease (dermatology/acne-vulgaris-folliculitis-and-pilonidal-disease).

Presenting picture. Centrocacial flushing and persistent redness, papules and pustules (without comedones), telangiectasia, sometimes phymatous skin or ocular symptoms. It is chronic and relapsing.

Most likely diagnosis. Rosacea, by phenotype. Exclude lupus erythematosus, seborrhoeic dermatitis, acne and steroid-induced rosacea.

Best first test. Clinical, with awareness that secondary syphilis can mimic a papulosquamous facial eruption in the right clinical context.

Best first treatment. Match treatment to the feature: alpha-agonist creams and laser for persistent erythema; ivermectin 1% cream once daily, metronidazole 0.75% twice daily or azelaic acid 15% twice daily for papules and pustules, with sub-antibiotic doxycycline 40 mg modified release for moderate or refractory disease. ^[16] Isotretinoin 0.25 to 0.3 mg per kg per day is reserved for difficult or phymatous disease. ^[16]

Commonest wrong answer. Calling rosacea "adult acne" and using benzoyl peroxide or harsh topicals that worsen redness; or overlooking ocular involvement.

Full topic: Rosacea and pityriasis rosea (dermatology/rosacea-and-pityriasis-rosea).

Presenting picture. Sudden patchy hair loss on the scalp or beard, with exclamation-mark hairs at the margins; total loss in alopecia universalis. Nail pitting occurs in up to 30%.

Most likely diagnosis. Alopecia areata, an autoimmune non-scarring alopecia.

Best first test. Clinical. Severe disease is graded (S1 to S5 by percentage hair loss). If shedding is diffuse, check thyroid function and iron status; if scarring is suspected, biopsy.

Best first treatment. Localised disease can be treated with intralesional triamcinolone acetonide (commonly 5 mg per ml) or a potent topical corticosteroid under occlusion. ^[13] Extensive disease needs dermatology and options such as baricitinib 2 or 4 mg by mouth daily and contact immunotherapy in selected patients. ^[13]

Commonest wrong answer. Reassuring a patient that the hair will "certainly come back" while missing totalis or the psychosocial burden, or biopsying every case.

Full topic: Hair and nail disorders (dermatology/hair-and-nail-disorders).

Presenting picture. Gradual patterned hair thinning in men (frontal recession and vertex) and in women (diffuse crown thinning with intact frontal hairline); acute diffuse shedding a few months after a stress, illness, childbirth or drug change.

Most likely diagnosis. Androgenetic alopecia or telogen effluvium.

Best first test. Clinical and history; pull test and dermoscopy help separate the two.

Best first treatment. Topical minoxidil and oral finasteride are the approved medical treatments for male pattern hair loss; telogen effluvium is managed by correcting the trigger and reassurance, with recovery over months.

Commonest wrong answer. Prescribing finasteride for women of childbearing potential without an appropriate specialist plan; or not explaining to someone with telogen effluvium that shedding is often self-limiting.

Full topic: Hair and nail disorders (dermatology/hair-and-nail-disorders).

Presenting picture. A thickened, discoloured, crumbly nail, usually toenail, often with subungual debris and distal onycholysis.

Most likely diagnosis. Onychomycosis, dermatophyte in 90% of toenail cases. Distinguish from trauma, psoriasis, lichen planus and chronic paronychia.

Best first test. Mycology (KOH and culture, or PCR where available) before committing to a long course.

Best first treatment. Oral terbinafine is the drug of choice: 250 mg once daily for 12 weeks for toenails and 6 weeks for fingernails, adjusted by weight in children. ^[14] Topical antifungal therapy is reserved for mild disease with fewer than 3 nails and less than 50% nail involvement. ^[14]

Commonest wrong answer. Treating a traumatised or psoriatic nail as fungal without confirming, or stopping oral terbinafine early because the nail still looks abnormal.

Full topic: Hair and nail disorders (dermatology/hair-and-nail-disorders).

Presenting picture. A red, swollen, tender nail fold, worse after wet work; in chronic disease there is rounding of the proximal nail fold, loss of the cuticle and Beau lines.

Most likely diagnosis. Acute (usually staphylococcal) or chronic (Candida and irritant) paronychia.

Best first test. Clinical; swab if infection is suspected or the case is recurrent.

Best first treatment. Keep the fingers dry, apply topical antifungal or corticosteroid, and treat bacterial infection with a systemic antibiotic when needed. Avoid prolonged water exposure.

Commonest wrong answer. Incising a chronic paronychia as if it were an abscess, or prescribing repeated antibiotics without addressing the wet-work trigger.

Full topic: Hair and nail disorders (dermatology/hair-and-nail-disorders).

Presenting picture. A painful, febrile, mucocutaneous eruption with confluent erythema, blistering and epidermal detachment, usually 5 to 28 days after starting a new drug (the Latin American guidelines state 5 to 28 days; some case reviews state 4 to 28 days). ^[4] There are oral, ocular and genital erosions.

Most likely diagnosis. SJS (small body surface area involvement) or TEN (widespread involvement); overlap syndrome between. Mortality in the acute phase ranges from 10 to 40 percent, depending on how much of the body surface is detached. ^[4]

Best first test. Clinical; biopsy shows full-thickness epidermal necrosis. Use the ALDEN algorithm to assess drug causality. The SCORTEN score predicts mortality on admission and should be reassessed on days 1 and 3. ^[4]

Best first treatment. Immediately stop the suspected drug; admit to intensive care or a burns unit; give supportive care with fluid replacement (larger volumes when more than 30% of the body surface is involved, targeting urine output of 0.5 to 1 ml per kg per hour), electrolyte monitoring, mucosal and ocular care and infection control. ^[4] There is no single proven disease-modifying drug; immunomodulatory therapy remains controversial.

Commonest wrong answer. Delaying drug withdrawal; treating the blisters with antibiotics alone; or waiting for a biopsy before stopping the drug.

Full topic: Drug eruptions, erythema multiforme and SJS/TEN (dermatology/drug-eruptions-and-severe-cutaneous-reactions).

Presenting picture. Severe pain out of proportion to the skin, rapidly spreading redness, swelling beyond the erythematous border, bullae, and skin colour change, sometimes with fever, tachycardia and hypotension.

Most likely diagnosis. Necrotising fasciitis. Mortality in acute disease is about 20 to 30%. ^[7]

Best first test. Clinical. Plain radiographs detect subcutaneous gas (specific but not sensitive, as gas is present in under 25%); rapid imaging can show fluid along fascial planes. ^[7]

Best first treatment. Resuscitate, give broad-spectrum intravenous antibiotics covering Gram-positive, Gram-negative and anaerobic organisms, and arrange emergency surgical debridement as soon as possible, with re-exploration every 12 to 24 hours. ^[7]

Commonest wrong answer. Waiting for imaging before operating, or relying on a "low-risk" LRINEC score to reassure.

Full topic: Impetigo, cellulitis and necrotising fasciitis (dermatology/bacterial-skin-infections-impetigo-cellulitis-necrotising).

Plain-text references to MedGrasp topics: Atopic dermatitis (dermatology/atopic-dermatitis); Contact, seborrhoeic and stasis dermatitis (dermatology/contact-seborrhoeic-and-stasis-dermatitis); Psoriasis (dermatology/psoriasis); Urticaria, angioedema and hypersensitivity reactions (dermatology/urticaria-and-hypersensitivity-reactions); Drug eruptions, erythema multiforme and SJS/TEN (dermatology/drug-eruptions-and-severe-cutaneous-reactions); Impetigo, cellulitis and necrotising fasciitis (dermatology/bacterial-skin-infections-impetigo-cellulitis-necrotising); Pemphigus vulgaris and bullous pemphigoid (dermatology/pemphigus-and-bullous-pemphigoid); Melanoma (dermatology/melanoma); Basal cell carcinoma, squamous cell carcinoma and Merkel (dermatology/keratinocyte-cancers-and-merkel-cell-carcinoma); Vitiligo and disorders of pigmentation (dermatology/vitiligo-and-pigment-disorders); Benign skin tumours and naevi (dermatology/benign-skin-tumours-and-naevi); Acne vulgaris, folliculitis and pilonidal disease (dermatology/acne-vulgaris-folliculitis-and-pilonidal-disease); Rosacea and pityriasis rosea (dermatology/rosacea-and-pityriasis-rosea); Hair and nail disorders (dermatology/hair-and-nail-disorders).