Scalp, nail and palmoplantar psoriasis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Scalp, nail, palm and sole psoriasis are high-impact sites where anatomy reduces topical access and a small affected area can cause severe disability. Good care begins by exposing the site fully and documenting what the person cannot do.

Diagnosis is usually clinical but common mimics are especially important here. Scalp scale can conceal tinea, nail dystrophy is not synonymous with fungus, and unilateral hyperkeratotic hand disease needs sampling before prolonged corticosteroid.

Management combines an acceptable vehicle, deliberate scale reduction, time-limited anti-inflammatory therapy and realistic review intervals. Nails improve slowly, while painful fissures and infection need earlier reassessment.

Key points

Scalp psoriasis forms sharply defined plaques with adherent scale, often extending beyond the hairline; part the hair and inspect ears, face, elbows and nails before deciding it is simple dandruff.
Nail matrix disease causes pitting, ridging or crumbling; nail-bed disease produces salmon or oil-drop change, onycholysis and subungual hyperkeratosis.
Palmoplantar plaques are thick, sharply bounded and fissured; palmoplantar pustulosis produces recurrent sterile pustules that become yellow-brown and is strongly associated with smoking.
Difficult-site severity is measured by pain, walking, hand use, sleep, work, appearance and distress, not by body surface area alone.
For scalp psoriasis, NICE starts with a potent topical corticosteroid once daily for up to four weeks, then checks technique, formulation and scale before changing therapy.
Do not prescribe oral antifungal treatment for a dystrophic nail without adequate microscopy and culture or another validated fungal test; psoriasis and fungus may coexist.
Major nail impact, uncontrolled palmoplantar disease or failure of properly used topical therapy merits dermatology referral and may meet criteria for phototherapy or systemic treatment.
Ask about joint, heel, digit and back symptoms: nail psoriasis increases suspicion, but skin or nail severity does not determine arthritis severity.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Shared psoriatic inflammation

Scalp, nail and palmoplantar disease arise from the same immune-mediated psoriatic process, but site anatomy changes morphology, treatment penetration and functional cost. Any phenotype may occur with little psoriasis elsewhere.

Mechanical amplification

Pressure, friction, repetitive hand work and trauma can aggravate palms, soles and nails through Koebnerisation. These exposures modify expression but do not make the disorder contagious or self-inflicted.

Palmoplantar pustulosis context

Palmoplantar pustulosis causes recurrent sterile pustules and is strongly associated with smoking. It can coexist with psoriasis, although its classification and response differ from ordinary thick palmoplantar plaque disease.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Hair-bearing barrier
Dense hair obstructs delivery to scalp skin while thick adherent scale limits penetration. Appropriate vehicles and descaling can therefore matter as much as nominal drug potency.
2
Nail-unit localisation
Matrix inflammation produces pitting, ridging and crumbling; nail-bed disease causes oil-drop change, onycholysis and subungual hyperkeratosis. Slow nail growth delays visible response for months.
3
Thick acral epidermis
Palmar and plantar stratum corneum reduces topical penetration, while load-bearing turns hyperkeratosis and fissures into pain and disability. Occlusion can improve penetration but also increases adverse-effect exposure.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Scalp plaque

Palpable, sharply marginated scale may cross the frontal hairline or sit behind ears. Examine the scalp surface after parting hair; alopecia is unusual unless traction, infection, picking or another scarring process coexists.

Nail matrix signs

Multiple irregular pits, transverse ridging, leukonychia and crumbling indicate matrix involvement. One altered nail has a broader structural or neoplastic differential than symmetric changes across several nails.

Nail-bed signs

Oil-drop or salmon-patch discolouration, distal onycholysis, splinter haemorrhages and subungual hyperkeratosis support nail-bed psoriasis. Avoid cutting back into attached nail or cleaning aggressively beneath it.

Palmoplantar plaque

Hyperkeratotic plaques have relatively sharp borders and painful fissures on load-bearing surfaces. Psoriasis elsewhere and nail changes support diagnosis; unilateral scale should heighten suspicion of tinea.

Palmoplantar pustules

Crops of non-infectious pustules arise on palms or soles, then become yellow-brown and scaly. Ask about smoking and bone or joint pain; fever or dissemination suggests a different, more urgent process.

Permanent-damage warningRed flag

Rapid nail loss, scarring hair loss, severe fissuring that prevents walking or a changing ulcerated acral lesion needs accelerated assessment rather than repeated empirical topical treatment.

Red flags requiring action

Painful fluctuant swelling, spreading warmth, purulent discharge or fever suggests bacterial infection and requires prompt severity and sepsis assessment.
Rapidly progressive nail destruction, scarring scalp alopecia or an ulcerated palmoplantar lesion needs expedited diagnostic review because permanent loss or malignancy is possible.
New generalised pustules, malaise or extensive skin inflammation requires same-day dermatology assessment rather than topical escalation.
Dactylitis, joint swelling, heel pain or inflammatory back pain may accompany nail psoriasis and should trigger rheumatology referral when psoriatic arthritis is suspected.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
First-line site examinationFirst stepFirst line
Why
Map scalp, nail-unit, palm and sole morphology and search for psoriasis at less symptomatic sites.
Interpretation and limitations
Concordant plaques, multiple psoriatic nail signs and symmetric acral disease increase confidence; asymmetry, hair loss, ulceration or absent supporting sites expands the differential.
02
Nail clippings and subungual debris for mycology
Why
Confirm or exclude fungal nail infection before committing to months of systemic antifungal therapy.
Interpretation and limitations
Sample the most proximal diseased material after cleaning contaminants. A negative result can reflect inadequate sampling, and positive fungus does not exclude concurrent psoriasis.
03
Skin scraping from active palm or sole scale
Why
Identify dermatophyte infection when disease is unilateral, annular, steroid-modified or otherwise atypical.
Interpretation and limitations
Microscopy supports earlier decisions while culture is slower; sample before antifungal treatment when safe because partial therapy reduces yield.
04
Nail Psoriasis Severity Index in specialist care
Why
Provide a reproducible baseline when nail disease has major functional or cosmetic impact or nail-specific treatment starts.
Interpretation and limitations
NAPSI measures signs, not the person's lived burden; pair it with pain, dexterity, work and patient-reported impact.
05
Psoriatic arthritis assessment
Why
Detect musculoskeletal disease associated with psoriasis, particularly in someone with nail involvement.
Interpretation and limitations
Use PEST for adult peripheral screening but ask independently about axial symptoms; refer when clinical suspicion exists regardless of normal inflammatory markers.
06
Biopsy or nail-unit specialist assessment
Why
Resolve a solitary destructive nail, scarring scalp process, ulcerated acral plaque or other discordant presentation.
Interpretation and limitations
Choose the diagnostic site with specialist input because nail-matrix and acral biopsies can scar; explain risks, obtain consent and give pathology a focused differential.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Scalp mimics

Seborrhoeic dermatitis has thinner greasy scale and typical facial involvement; tinea capitis may cause broken hairs, lymphadenopathy or inflammatory kerion; contact allergy follows product exposure.

Onychomycosis

Fungal nail disease can produce thickening, discolouration and onycholysis and may coexist with psoriasis. Obtain good-quality nail material before oral antifungal treatment rather than diagnosing by appearance alone.

Hand and foot eczema

Irritant or allergic dermatitis, pompholyx and hyperkeratotic eczema can resemble palmoplantar psoriasis. Exposure history, vesicles, border, other psoriasis signs and targeted patch or fungal testing refine probability.

Local structural disease

Lichen planus, alopecia areata, trauma and tumours can alter one nail; keratoderma, warts and keratinising malignancy can mimic a focal acral plaque. Asymmetry and ulceration warrant reconsideration.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-lineScalp treatment sequenceFirst stepFirst lineConfirmed scalp psoriasis without infection or scarring alopecia.

1Part the hair, loosen thick adherent scale with salicylic-acid, oil or emollient preparation where appropriate, then wash out gently rather than picking plaques.
2Apply a potent topical corticosteroid scalp formulation once daily for up to four weeks, directing it onto skin rather than coating hair.
3At four weeks, check quantity, technique and acceptability; if response is inadequate, try another potent-steroid formulation and/or deliberate descaling before assuming pharmacological failure.
4After a further inadequate four-week approach, NICE offers once-daily calcipotriol/betamethasone combination for up to four weeks, or once-daily vitamin-D analogue for mild-to-moderate disease when steroid cannot be used.

02Nail pathwaySlow-growth shared decisionNail psoriasis causing pain, functional restriction or important cosmetic distress.

1Confirm which nail compartment is involved, photograph a baseline, keep nails short without traumatic cleaning, and test for fungus when appearance or treatment plan makes it relevant.
2Explain that topical treatment must reach matrix or nail bed and visible improvement follows nail growth, so a meaningful trial takes months rather than days.
3Refer when several nails, rapid progression, diagnostic uncertainty or major function is involved; systemic eligibility can be based on severe local impact even when skin extent is small.

03Palmoplantar pathwayRestore barrier and functionHyperkeratotic plaque or localised palmoplantar pustulosis without systemic upset.

1Reduce friction, protect fissures, use generous greasy emollient and consider a keratolytic for thick scale; address smoking support in palmoplantar pustulosis without blame.
2Use potent or specialist-supervised very potent corticosteroid for a short defined course; employ occlusion only when specifically prescribed because it markedly increases absorption.
3Refer early for walking or hand-function loss, repeated topical failure or pustular disease; NICE considers local PUVA for palmoplantar pustulosis and systemic treatment for severe high-impact local disease.

04EscalationRecheck diagnosis before adding potencyEscalationUnexpected treatment failure, asymmetric disease, destructive change or signs of infection or arthritis.

1Repeat examination and obtain fungal material or bacterial culture when indicated before further immunosuppressive topical treatment.
2Expedite dermatology for scarring alopecia, destructive nail disease, ulceration or major functional impact; suspected cancer follows the appropriate urgent referral pathway.
3Refer suspected psoriatic arthritis to rheumatology as soon as it is recognised and use immediate same-day assessment for generalised pustules, erythroderma or systemic illness.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

NICE first-line active treatment for scalp psoriasis, with technique teaching and descaling where adherent scale blocks delivery.

Potent topical corticosteroid scalp formulation

Apply a thin layer to affected scalp skin once daily for up to 4 weeks, using the formulation and maximum quantity specified for the prescribed product.

Avoid face and eyes, infected skin and uncontrolled prolonged use; review for atrophy, folliculitis or inadequate delivery, and remember flammable residue with some vehicles.

A licensed fixed combination for stable adult plaque psoriasis and a NICE once-daily option after specified topical steps; product formulation determines suitable sites.

Calcipotriol 50 micrograms/g plus betamethasone 0.5 mg/g ointment

Apply once daily to affected adult plaque psoriasis for 4 weeks; do not exceed 15 g daily or treat more than 30% body surface area with calcipotriol-containing products.

Avoid face, flexures, genitals, calcium-metabolism disorders, severe renal or hepatic impairment and generalised pustular or erythrodermic disease; wash hands and avoid excess ultraviolet exposure.

Specialist-supervised short treatment for resistant steroid-responsive plaques on thick palmar or plantar skin after diagnosis and infection review.

Very potent topical corticosteroid for thick palmoplantar plaques

Apply clobetasol propionate 0.05% thinly once or twice daily for the shortest course needed, stopping or stepping down by 4 weeks; maximum 50 g weekly.

Not for widespread plaque psoriasis, untreated infection or unsupervised occlusion; greater area, inflammation and covering increase systemic absorption and adrenal-suppression risk.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Functional impairment

Fissured soles impair walking, painful fingertips limit dexterity, and severe nail disease disrupts work and self-care. NICE recognises localised functional impairment as a reason to consider systemic treatment eligibility.

Permanent nail damage

Persistent matrix inflammation can scar or deform nails, while aggressive clipping and picking worsen onycholysis. Early specialist input is appropriate when change is rapid or highly disabling.

Secondary infection

Fissures, detached nail and excoriated scalp permit bacterial or fungal entry. Infection should be treated on clinical and microbiological grounds, not assumed from every crust or discoloured nail.

Cumulative topical harm

Unreviewed very potent steroid, inappropriate occlusion and excessive calcipotriol can cause local or systemic toxicity. Hair products and greasy emollients also carry transfer and fire-safety concerns.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review scalp treatment by four weeks to inspect skin directly, confirm the medicine reaches plaques, quantify use and adjust formulation or descaling before escalating the drug class.
Photograph nails and record symptoms, NAPSI where appropriate and patient-valued functions; allow for slow nail growth but reassess sooner if pain, infection or destruction progresses.
Track palmoplantar fissures, walking, grip, work and secondary infection alongside visible scale or pustules; a modest area can still justify specialist treatment.
Ask annually about psoriatic arthritis and at every relevant change; document PEST plus axial symptoms rather than relying on the questionnaire alone.
Adults receiving intermittent potent or very potent steroid need at least annual review for local adverse effects, with more frequent review after occlusion or high cumulative quantities.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Vehicle is an intervention

A lotion, gel, foam or scalp application reaches hair-bearing skin more reliably than a disliked ointment. Ask how and when the person can apply it.

Matrix versus bed

Pitting points towards matrix inflammation, whereas oil-drop change and onycholysis arise from the bed. The anatomical target explains why topical access and response differ.

Fungus can coexist

A positive fungal sample does not erase psoriatic nail signs elsewhere. Treat confirmed infection and reassess the residual nail phenotype as growth replaces diseased plate.

Pustules are not automatically infection

Palmoplantar pustulosis is sterile, but painful spreading warmth, purulent drainage or fever still warrants infection assessment. Morphology and systemic context determine urgency.

Occlusion changes the dose

A glove, dressing or cling film can substantially increase corticosteroid penetration. It should be a deliberate prescribed method with duration and safety review, not an improvised intensifier.

11Common pitfallsFrequent interpretation and management errors.

01
Calling scalp scale dandruff without exposing the skin or checking the hairline, ears, extensor surfaces and nails.
02
Diagnosing onychomycosis visually and prescribing prolonged oral antifungal treatment without an adequate specimen.
03
Judging difficult-site psoriasis mild because the affected body surface area is small.
04
Applying scalp medicine mainly to hair, then labelling an appropriate drug ineffective.
05
Using potent steroid under improvised occlusion without accounting for increased absorption and infection risk.
06
Missing inflammatory back pain because a PEST questionnaire is negative.