Skin & Subcutaneous Tissue

Seborrheic dermatitis: diagnosis and management

Clinical Overview and When to Suspect Seborrheic Dermatitis

— Infantile form (cradle cap): peaks 3 weeks–3 months, self-limited, resolves by 8–12 months.

— Adult form: peaks 30–60 years, male predominance, chronic course with flares.

— Cold/dry weather, stress, sleep deprivation, sweating, alcohol

— Drugs: lithium, buspirone, haloperidol, interferon, psoralens, gold

— Neurologic disease: Parkinson disease, post-stroke, spinal cord injury, tardive dyskinesia (likely from increased sebum pooling and decreased facial movement)

— Immunosuppression: HIV/AIDS (prevalence up to 35–85%), organ transplant, chemotherapy

— Adult with chronic, recurrent greasy yellow scale on scalp, nasolabial folds, eyebrows, glabella, ears, chest, or intertriginous areas

— Infant with non-pruritic, yellow, crusted scalp scale

— Patient with new-onset severe or refractory SD → screen for HIV and consider underlying neurologic disease

Seborrheic dermatitis (SD) is a chronic, relapsing inflammatory dermatosis of sebum-rich skin driven by an inflammatory response to Malassezia yeast (especially M. globosa and M. restricta) in genetically predisposed hosts.

Prevalence ~3–5% of adults; "dandruff" (pityriasis capitis) is the mild scalp form and affects up to 50% of adults at some point.

Bimodal age distribution:

Triggers and exacerbators:

When to suspect on Step 3:

Board pearl: Sudden, explosive, or treatment-resistant seborrheic dermatitis in a young adult is an AIDS-defining clinical clue—offer HIV testing. Similarly, new severe SD in an older adult should prompt evaluation for parkinsonism.

Key distinction: SD is not caused by poor hygiene, and Malassezia is normal flora—the disease reflects host inflammatory response, not infection per se, which is why antifungals and anti-inflammatories both work.

Course: chronic with waxing/waning flares; counsel patients early that this is a control, not cure, condition managed long-term in the outpatient setting.

Presentation Patterns and Key History

— Mild-to-moderate pruritus (scalp itch most common complaint)

— Burning or stinging on the face, especially with shaving or skincare

— Visible flaking ("dandruff") embarrassing to patient—often the chief complaint

— Worsening in winter, improvement with sun exposure (UV suppresses Malassezia)

— Scalp: diffuse fine white-to-yellow scale (dandruff) → thick adherent greasy plaques

— Face: nasolabial folds, glabella, medial eyebrows, beard area, retroauricular sulci, external auditory canal (otitis externa-like)

— Trunk: petaloid (flower-petal) plaques on presternal chest and interscapular back

— Intertriginous: axillae, inframammary, umbilicus, inguinal folds, gluteal cleft (inverse SD)

— Eyelids: seborrheic blepharitis with greasy lid margins and collarettes

— Onset 2–10 weeks; asymptomatic, non-pruritic (key contrast to atopic dermatitis)

— Thick adherent yellow scalp scale ± diaper area, neck folds, retroauricular involvement

— Medication list (lithium, interferons, EGFR inhibitors)

— Neurologic symptoms (tremor, gait change, bradykinesia)

— HIV risk factors and last test date

— Atopic history (asthma, allergic rhinitis, AD) to weigh differential

— Prior treatment response (especially to ketoconazole or zinc shampoos)

Take a focused history targeting distribution, chronicity, triggers, and red-flag comorbidities.

Cardinal symptoms:

Distribution patterns by site:

Infantile SD history:

Targeted history to obtain:

Step 3 management: In a 28-year-old man with abrupt severe facial and chest SD plus weight loss or lymphadenopathy, order a fourth-generation HIV Ag/Ab combination assay the same visit—do not just refer to dermatology.

Board pearl: Infantile SD is non-pruritic; an itchy, miserable infant with similar distribution is far more likely atopic dermatitis—pruritus is the single best discriminating symptom on the stem.

Physical Exam Findings

— Erythematous patches and thin plaques with overlying greasy, yellow-to-white, branny scale

— Ill-defined borders (contrast with sharply demarcated psoriasis)

— No vesicles, no oozing (if present, consider superinfection or contact dermatitis)

— Scalp: diffuse fine scale ± erythema; thick yellow crusts in severe cases; minimal hair loss (telogen effluvium possible but no scarring alopecia)

— Face: symmetric pink-red patches in nasolabial folds, glabella, medial brows; eyebrow scale ("seborrheic brows")

— Ears: scaling in conchal bowl, posterior auricular sulcus, external canal—a commonly missed site

— Trunk: oval pink petaloid plaques on presternum; less commonly annular/figurate patterns

— Eyelids: erythematous, scaly lid margins with retained scales at base of lashes

— Thick, adherent, yellow-to-brown greasy scalp scale (cradle cap)

— Salmon-pink patches in diaper area, neck creases, axillae—typically non-excoriated

— Extent (% BSA) and impact on quality of life

— Signs of superinfection: honey crusts (impetigo), pustules (candida in folds)

— Erythroderma in HIV or immunocompromised—a red flag

— KOH if tinea suspected (esp. scalp in children → consider tinea capitis)

— Wood lamp for pigmentary changes

— Biopsy only for atypical or refractory cases

SD is a clinical diagnosis—a careful skin exam under good lighting almost always suffices.

Primary lesions:

Site-specific findings:

Infantile exam:

Examine for severity and complications:

Diagnostic maneuvers (rarely needed):

Key distinction: Psoriasis scale is silvery, thick, micaceous, with sharp borders and Auspitz sign; SD scale is greasy, yellow, and poorly demarcated. Overlap exists ("sebopsoriasis"), particularly on the scalp.

Board pearl: Involvement of the external auditory canal and retroauricular sulcus is highly characteristic of SD and frequently overlooked—always lift the ear during exam.

Diagnostic Workup — Initial Labs and Studies

— Atypical distribution or morphology

— Severe, refractory, or rapidly progressive disease

— Diagnostic uncertainty (psoriasis, tinea, cutaneous lupus, secondary syphilis)

— Suspicion of underlying immunosuppression or neurologic disease

— HIV Ag/Ab combination assay (4th-generation): any young adult with severe, sudden-onset, or refractory SD; CD4 count and viral load if positive

— KOH scraping: rules out tinea capitis (children) or tinea faciei/corporis

— Bacterial culture: pustular or weeping lesions suggesting superinfection

— TSH if concomitant signs of thyroid dysfunction (myxedema can mimic)

— Nutritional labs: zinc, biotin, niacin, riboflavin, and EFAs in infants with FTT or refractory SD-like rash (zinc deficiency → acrodermatitis enteropathica)

— In older adults with new-onset severe facial SD, look for bradykinesia, masked facies, rest tremor, cogwheel rigidity—refer to neurology if Parkinson disease suspected

— Persistent infantile SD beyond 12 months or with FTT → consider Langerhans cell histiocytosis (purpuric papules, ear discharge, hepatosplenomegaly), zinc deficiency, immunodeficiency

— Spongiosis, parakeratosis at follicular ostia, neutrophils in scale crust, superficial perivascular lymphocytic infiltrate—nonspecific but supportive

Seborrheic dermatitis is a clinical diagnosis—no routine labs, imaging, or skin biopsy are required for typical presentations.

When to obtain ancillary testing:

Targeted workup based on red flags:

Neurologic evaluation:

Pediatric considerations:

Biopsy findings (if performed):

Step 3 management: Order HIV testing in any adult with severe or treatment-resistant SD before escalating to systemic therapy—the diagnosis fundamentally changes management and prognosis, and you do not want to start systemic steroids in undiagnosed HIV.

Board pearl: A scaly, "seborrheic-looking" rash in an infant with hepatosplenomegaly, purpura, or chronic otorrhea is Letterer-Siwe (LCH) until proven otherwise—biopsy required.

Diagnostic Workup — Advanced or Confirmatory Studies

— Indicated when psoriasis, cutaneous T-cell lymphoma, discoid lupus, pemphigus foliaceus, or LCH cannot be excluded clinically

— Histopathology: spongiotic dermatitis with shoulder parakeratosis around follicular ostia, lymphocytic exocytosis, and neutrophils within parakeratotic scale—the latter helps distinguish from simple eczema

— Direct immunofluorescence to exclude autoimmune blistering disease if pemphigus considered

— KOH prep of scale: scattered yeast forms (Malassezia) are normal flora and do not confirm SD—presence is expected; absence of dermatophyte hyphae helps exclude tinea

— Fungal culture on Sabouraud agar with olive oil overlay if tinea capitis suspected in children

— Consider when facial dermatitis is refractory to standard SD therapy—allergic contact dermatitis to fragrance, methylisothiazolinone, or hair products can mimic or coexist

— SD: arborizing/atypical vessels, yellowish scales, no perifollicular scaling

— Psoriasis: red dots and globules, regular punctate vessels, silvery scale

— Tinea capitis: comma hairs, corkscrew hairs, broken hairs

— ANA, anti-Ro/SSA: subacute cutaneous lupus mimicking facial SD

— RPR/VPDRL: secondary syphilis (palms, soles, mucous patches—a "great mimicker")

— HIV with CD4 count: severe or recalcitrant disease

Reserved for atypical, refractory, or diagnostically uncertain cases.

Skin biopsy (4-mm punch):

Mycologic studies:

Patch testing:

Dermoscopy (trichoscopy of scalp):

Serologic testing when differential demands:

Imaging: virtually never indicated for SD itself; cross-sectional imaging only when systemic disease (LCH, lymphoma) suspected.

Key distinction: Malassezia on KOH is not diagnostic—it's commensal. Diagnosis remains clinical; mycology is for exclusion of dermatophytes, not confirmation of SD.

Board pearl: Refractory facial "SD" in a woman with photosensitivity, arthralgias, and annular plaques—obtain ANA and anti-Ro; subacute cutaneous lupus is frequently misdiagnosed as seborrheic dermatitis for years.

Risk Stratification and First-Line Management Logic

— Mild (dandruff or limited facial scale): OTC antifungal shampoo + gentle skincare

— Moderate (visible erythema and scale, symptomatic): prescription antifungal + short-course topical corticosteroid or calcineurin inhibitor

— Severe/refractory (extensive, eroded, immunocompromised): combination topical therapy ± oral antifungal; dermatology referral

— Reduce visible scale and erythema

— Control pruritus and burning

— Prolong remission intervals

— Minimize topical steroid exposure on face

— Address psychosocial impact (self-esteem, work, intimacy)

— Gentle, non-soap cleansers; avoid harsh scrubs and astringents

— Avoid alcohol-based toners and fragranced products

— Sunlight in moderation can help (UV suppresses Malassezia)—but balance with photoprotection

— Stress management and adequate sleep

— Smoking cessation (smoking is an independent risk factor)

— Scalp: medicated shampoo (ketoconazole 2%, ciclopirox 1%, selenium sulfide 2.5%, zinc pyrithione 1–2%) used 2–3× weekly, lather 5 minutes before rinse

— Face/intertriginous: ketoconazole 2% cream or ciclopirox gel BID; add low-potency steroid (hydrocortisone 1–2.5%) or topical calcineurin inhibitor for flares

— Trunk: ketoconazole cream + low- to mid-potency steroid short course

Treatment intensity is matched to disease severity, distribution, and patient factors.

Severity tiers and stepwise approach:

Treatment goals (set with patient):

General measures for all patients:

Workflow by site:

Step 3 management: For a working adult with moderate scalp and facial SD, prescribe ketoconazole 2% shampoo (scalp, 3×/week) + ketoconazole 2% cream (face, BID for 4 weeks) + hydrocortisone 2.5% cream (face, BID for 1 week only), then maintenance antifungal alone. Counsel that improvement takes 2–4 weeks.

Board pearl: Topical calcineurin inhibitors (tacrolimus 0.1%, pimecrolimus 1%) are preferred over chronic steroids on the face and intertriginous areas to avoid atrophy, telangiectasias, and perioral dermatitis.

Pharmacotherapy — First-Line Drug Regimen

— Ketoconazole 2% shampoo/cream/foam: most evidence; BID for cream, 2–3×/week for shampoo

— Ciclopirox 1% shampoo, 0.77% gel/cream: dual antifungal + anti-inflammatory

— Selenium sulfide 2.5% shampoo: effective, can bleach hair/jewelry

— Zinc pyrithione 1–2% shampoo: OTC, well-tolerated

— Coal tar shampoos: keratolytic + antiproliferative; messy, photosensitizing

— Face/folds: hydrocortisone 1–2.5% BID × 5–7 days

— Scalp: clobetasol 0.05% solution/foam or fluocinolone 0.01% oil, short bursts

— Trunk: triamcinolone 0.1% cream BID, max 2 weeks

— Avoid chronic facial use → atrophy, telangiectasias, perioral dermatitis, steroid rosacea

— Tacrolimus 0.1% ointment or pimecrolimus 1% cream BID

— Off-label for SD but well-supported; safe for long-term maintenance

— Counsel about transient burning and FDA boxed warning (theoretical malignancy risk, largely unsubstantiated)

— Roflumilast 0.3% foam (PDE4 inhibitor): FDA-approved 2023 for SD ≥9 years old; non-steroidal, once daily

— Salicylic acid shampoos or oils; warm mineral oil with gentle brushing for cradle cap

— Itraconazole 200 mg daily × 1 week, then 200 mg/day × 2 days/month maintenance

— Fluconazole 150–300 mg weekly × 2–4 weeks (alternative)

— Check LFTs; watch drug interactions (CYP3A4)

Three pharmacologic pillars: antifungals, anti-inflammatories (steroids/calcineurin inhibitors), and keratolytics.

Topical antifungals (mainstay):

Topical corticosteroids (for flares only):

Topical calcineurin inhibitors (steroid-sparing, ideal for face):

Newer agents:

Keratolytics for thick scale:

Oral antifungals (severe/refractory adults only):

CCS pearl: In a CCS-style outpatient case, advance the clock by 4 weeks after initial regimen and reassess; if persistent, add tacrolimus 0.1% ointment BID rather than continuing topical steroids on the face.

Board pearl: Roflumilast foam is the highest-yield "new drug" answer for facial/scalp SD in patients wanting to avoid steroids and calcineurin inhibitors.

Expanded Pharmacology and Refractory Disease Management

— Is shampoo being left on 5 minutes before rinsing?

— Frequency: 2–3×/week for maintenance, daily during flares

— Rotating between agents (e.g., ketoconazole and zinc pyrithione) reduces tachyphylaxis

— Treating all involved sites (often face is treated but scalp neglected)

— Antifungal cream BID + calcineurin inhibitor BID alternating with antifungal shampoo on scalp

— Add short pulse of mid-potency steroid for acute flares (≤2 weeks)

— Erythrodermic SD

— HIV-associated severe SD unresponsive to topicals

— Disabling, widespread disease impairing function or QoL

— Itraconazole 200 mg daily × 1 week → maintenance 200 mg/day × 2 consecutive days each month (most evidence)

— Fluconazole 300 mg/week × 2–4 weeks

— Terbinafine 250 mg daily × 4–6 weeks (less effective for Malassezia than azoles)

— Avoid ketoconazole oral (hepatotoxicity, adrenal suppression—FDA restricted)

— Itraconazole/fluconazole + statins, warfarin, benzodiazepines, calcium-channel blockers, DOACs

— Check QT-prolonging combinations

— Narrowband UVB 3×/week for refractory, widespread disease

— Limited by access and time commitment

— Tea tree oil 5% shampoo (modest evidence)

— Topical lithium succinate/gluconate (Europe)

— Promiseb (non-steroidal device, contains piroctone olamine)

When standard topical therapy fails after 8–12 weeks of adherent use, escalate systematically.

Verify adherence and technique first:

Combination topical regimens for moderate-severe disease:

Systemic therapy indications:

Oral antifungal regimens:

Drug interactions to screen:

Phototherapy:

Adjunctive measures:

Step 3 management: For HIV-associated severe SD with CD4 <200, the single most effective intervention is initiating/optimizing ART—immune reconstitution dramatically improves SD. Combine with topical ketoconazole + tacrolimus while CD4 recovers.

Board pearl: Never prescribe oral ketoconazole for SD—hepatic failure and adrenal insufficiency risk; itraconazole is the preferred systemic azole.

Special Populations — Elderly and Renal/Hepatic Impairment

— Screen for Parkinson disease, post-stroke, dementia—facial immobility and sebum pooling drive SD; treating SD does not treat the underlying disorder, but improved facial mobility (e.g., with levodopa) often improves SD

— Caregivers may need education on shampoo application and facial care for dependent patients

— Thinner, more fragile skin → use low-potency steroids only and shorter courses to avoid purpura, atrophy, and tears

— Polypharmacy review: lithium, neuroleptics, interferons may be contributors

— Topical therapy: no dose adjustment for ketoconazole, ciclopirox, calcineurin inhibitors—minimal systemic absorption

— Oral fluconazole: reduce dose by 50% if CrCl <50 mL/min

— Oral itraconazole: use cautiously; capsule form preferred over solution (cyclodextrin vehicle accumulates in renal failure)

— Avoid IV itraconazole if CrCl <30

— Oral azoles (itraconazole, fluconazole, terbinafine) are hepatotoxic—obtain baseline LFTs, recheck at 4–6 weeks

— Avoid oral antifungals in Child-Pugh B/C cirrhosis; rely on topicals

— Terbinafine contraindicated in chronic or active liver disease

— Itraconazole: negative inotrope, contraindicated in heart failure (FDA boxed warning) for onychomycosis indication—use caution generally

— QT prolongation with fluconazole + other QT drugs (ondansetron, methadone, certain antipsychotics)

— Prefer shampoo-based therapy and gentle creams over alcohol-based gels/foams (sting on fragile skin)

— Address scalp care in nursing home residents—often neglected, contributing to thick crusts and secondary infection

SD prevalence rises in older adults, particularly those with neurologic disease, immobility, or polypharmacy.

Geriatric considerations:

Renal impairment:

Hepatic impairment:

Cardiac comorbidity:

Practical geriatric workflow:

CCS pearl: In an 82-year-old man with Parkinson disease and facial SD, order ketoconazole 2% cream BID, hydrocortisone 1% short-course, optimize Parkinson regimen with neurology, and counsel caregivers on scalp hygiene—a multi-pronged note that reflects Step 3 longitudinal care.

Special Populations — Pregnancy, Pediatrics, and Other Subgroups

— SD may flare or improve during pregnancy due to hormonal shifts

— Safe topicals: zinc pyrithione, selenium sulfide, ciclopirox shampoo, low-potency hydrocortisone in limited areas

— Ketoconazole shampoo: minimal absorption, considered safe; ketoconazole cream acceptable

— Avoid: oral azoles (fluconazole >150 mg single dose has dose-dependent teratogenicity—Category D at high cumulative doses), oral terbinafine (limited data), salicylic acid (>2%) over large areas

— Calcineurin inhibitors: limited data, use with caution; topical pimecrolimus has more reassuring registry data

— Breastfeeding: do not apply topicals directly to nipple/areola; wash before nursing if applied to chest

— First line: emollients—mineral oil, petrolatum, or vegetable oil applied 15–60 min before gentle brushing with soft brush, then mild baby shampoo

— Second line: ketoconazole 2% shampoo 2×/week (well-tolerated), low-strength hydrocortisone 1% for inflammatory areas (short courses)

— Avoid: salicylic acid (percutaneous absorption → salicylism), high-potency steroids, oral antifungals

— Reassure parents: self-limited, resolves by 8–12 months

— Diaper-area SD: ketoconazole cream + hydrocortisone 1% short course; rule out candida coinfection

— Differentiate from acne and atopic dermatitis; address self-esteem and treatment adherence

— Roflumilast foam approved ≥9 years old

— Prevalence up to 85% with AIDS; severity inversely correlates with CD4

— Initiate/optimize ART as central intervention

— Aggressive topical antifungals + calcineurin inhibitors; consider oral itraconazole

Pregnancy and lactation:

Infantile seborrheic dermatitis (cradle cap):

Adolescents:

HIV/immunocompromised:

Board pearl: In pregnancy, prefer ketoconazole 2% shampoo for scalp and hydrocortisone 1% short course for face—avoid oral antifungals, especially fluconazole, which is associated with cardiac, craniofacial, and skeletal malformations at high doses (Category D).

Complications and Adverse Outcomes

— Secondary bacterial infection (Staph aureus): honey-colored crusting, pustules → topical or oral antibiotics

— Secondary candidiasis in intertriginous SD: satellite pustules, fiery erythema → add topical azole + nystatin

— Erythroderma (>90% BSA): rare, risk in HIV/immunosuppressed → hospitalize for fluid/electrolyte management, temperature regulation

— Otitis externa: from canal SD; treat with ketoconazole + low-potency steroid ear drops

— Blepharitis and meibomian gland dysfunction: dry eye, chalazia—warm compresses, lid hygiene, refer to ophthalmology if visual symptoms

— Psychosocial morbidity: depression, anxiety, social avoidance—screen with PHQ-2

— Topical steroid atrophy, telangiectasias, striae: face and folds most vulnerable—limit potent steroids to ≤2 weeks

— Perioral dermatitis / steroid rosacea: from chronic facial steroid use—stop steroid, transition to tacrolimus, may need oral doxycycline

— Tachyphylaxis to topical steroids: rotate or step down

— Calcineurin inhibitor burning: transient, resolves over 1–2 weeks; pretreatment with cool compress helps

— Selenium sulfide: discoloration of light hair, jewelry

— Coal tar: photosensitivity, folliculitis, staining

— Oral itraconazole: hepatotoxicity, heart failure exacerbation, drug interactions

— Oral fluconazole: QT prolongation, hepatotoxicity

— Persistent "SD" beyond 12 months, hepatosplenomegaly, purpura, FTT, chronic otorrhea → biopsy to exclude Langerhans cell histiocytosis

Although SD itself is benign, complications arise from disease, treatment, or both.

Disease-related complications:

Treatment-related adverse effects:

Pediatric complication red flags:

Key distinction: Sudden worsening with honey-crusted lesions = impetiginization (Staph aureus), treat with mupirocin or oral cephalexin—do not simply intensify topical steroid.

Step 3 management: When a patient develops perioral dermatitis after months of clobetasol on the face, stop the steroid immediately (warn about rebound), start pimecrolimus or tacrolimus, add doxycycline 100 mg daily × 6–8 weeks if persistent papulopustular component.

When to Escalate Care — Consult, Referral, or Inpatient Triage

— Diagnosis uncertain after thorough exam

— Failure of 8–12 weeks of guideline-concordant therapy

— Erythrodermic, pustular, or atypical morphology

— Recurrent perioral dermatitis or steroid-induced rosacea

— Need for biopsy, patch testing, or phototherapy

— Pediatric SD with atypical features (suspect LCH or immunodeficiency)

— Seborrheic blepharitis with visual changes, persistent dry eye, or recurrent chalazia

— Eyelid involvement unresponsive to lid hygiene + warm compresses

— New facial SD in older adult with bradykinesia, rest tremor, masked facies, micrographia—evaluate for Parkinson disease

— Newly diagnosed HIV from SD workup → link to care same day when possible

— Severe SD with CD4 <200, opportunistic infections

— Erythrodermic SD: fluid loss, electrolyte abnormality, temperature dysregulation, high-output cardiac failure risk

— Severe secondary infection with systemic signs (cellulitis, bacteremia)

— Stevens-Johnson syndrome from misdiagnosed drug eruption

— Significant depression, anxiety, or body dysmorphic features driven by visible skin disease

— Use PHQ-9 / GAD-7 in clinic; SSRIs and CBT as appropriate

— Send a clear handoff note: prior topical regimens, duration, response, allergies, comorbidities, HIV status

— Document shared decision-making about steroid risks

Most SD is managed entirely in the outpatient primary care setting—escalation is uncommon but predictable.

Refer to dermatology when:

Refer to ophthalmology when:

Refer to neurology when:

Refer to infectious disease / initiate HIV care when:

Hospitalization indications (rare):

Mental health referral:

Care coordination:

CCS pearl: On a CCS case, when erythroderma is suspected, admit, place IV access, order CBC, BMP, albumin, thermoregulation support, dermatology consult, and broad-spectrum antibiotics if febrile—do not manage as outpatient.

Board pearl: New severe SD + oral thrush + weight loss in a young adult = HIV until proven otherwise—order HIV 4th-gen Ag/Ab before referral.

Key Differentials — Same-Category (Inflammatory Papulosquamous) Causes

— Silvery, thick, micaceous scale; sharp, well-demarcated borders

— Extensor surfaces (elbows, knees), umbilicus, gluteal cleft

— Nail pitting, oil drops, onycholysis; arthritis (dactylitis, DIP involvement)

— Auspitz sign (pinpoint bleeding on scale removal)

— Overlap "sebopsoriasis" exists—treat with combined antifungal + steroid; refer if uncertain

— Intensely pruritic (key contrast with SD, especially in infants)

— Flexural surfaces in children/adults; cheeks and extensors in infants

— Personal/family history of atopy (asthma, allergic rhinitis)

— Lichenification from chronic scratching

— Annular, scaling plaques with central clearing and active border

— Tinea capitis: scaly patches with broken hairs, alopecia, posterior cervical lymphadenopathy in children

— KOH-positive, fungal culture confirms

— Herald patch followed by "Christmas tree" distribution on trunk along skin lines

— Salmon-colored oval plaques with collarette scale; self-limited 6–8 weeks

— Central facial erythema, telangiectasias, papules, pustules

— Flushing triggers (alcohol, spicy food, heat)

— No scale (vs SD); can be exacerbated by topical steroid misuse

— Hypopigmented or hyperpigmented scaly macules on trunk/upper arms

— KOH: "spaghetti and meatballs" (Malassezia hyphae + spores)

Differentiating SD from other papulosquamous disorders is a high-yield Step 3 task.

Psoriasis (especially scalp and inverse):

Atopic dermatitis:

Tinea capitis / tinea faciei:

Pityriasis rosea:

Rosacea (papulopustular and erythematotelangiectatic):

Pityriasis versicolor:

Key distinction: Same Malassezia organism causes both SD and pityriasis versicolor, but versicolor is macular and trunk-predominant while SD is plaque-based on sebum-rich areas.

Board pearl: If "psoriasis vs SD" is the stem—look at the scale (silvery vs greasy yellow), borders (sharp vs ill-defined), and nails (pitting vs normal); nail findings essentially clinch psoriasis.

Key Differentials — Other-Category Causes

— Geographic, asymmetric distribution following exposure (hair dye, fragrance, nickel)

— Vesicles, weeping more prominent

— Patch testing diagnostic

— Photodistributed annular or papulosquamous plaques on V of neck, upper back, arms

— ANA, anti-Ro/SSA positive

— Often drug-induced (HCTZ, terbinafine, PPIs, calcium-channel blockers)

— Diffuse copper-colored maculopapular rash including palms and soles

— Mucous patches, condylomata lata, generalized lymphadenopathy

— RPR/VDRL with confirmatory treponemal test

— Heliotrope rash (violaceous eyelid edema), Gottron papules, shawl sign

— Proximal muscle weakness, elevated CK, ANA, anti-Jo-1, anti-Mi-2

— Superficial erosions with scale-crusts on seborrheic areas (mimics SD)

— Positive DIF (intercellular IgG, "chicken wire")

— Persistent "cradle cap" + purpura, hepatosplenomegaly, lytic bone lesions, otorrhea

— Biopsy: CD1a+, S100+, Birbeck granules

— Periorificial and acral dermatitis, diarrhea, alopecia in infants

— Low serum zinc; replace zinc orally

— Thick, asbestos-like scale on scalp—often a reaction pattern in SD, psoriasis, or tinea

— Lithium, interferons, EGFR inhibitors can cause SD-like eruption

When morphology and distribution are atypical, broaden beyond papulosquamous disorders.

Allergic / irritant contact dermatitis:

Subacute cutaneous lupus erythematosus (SCLE):

Secondary syphilis:

Dermatomyositis:

Pemphigus foliaceus:

Langerhans cell histiocytosis (infant/child):

Acrodermatitis enteropathica (zinc deficiency):

Tinea amiantacea:

Drug eruptions:

Key distinction: Palms and soles involved → think syphilis, not SD. SD essentially never involves palms/soles.

Board pearl: A patient on hydrochlorothiazide with photodistributed "SD-like" facial rash and a positive anti-Ro—the diagnosis is drug-induced SCLE; stop the HCTZ and start sun protection ± hydroxychloroquine.

Secondary Prevention and Long-Term Maintenance Plan

— Antifungal shampoo 1–2×/week indefinitely even when clear (ketoconazole 2%, ciclopirox, zinc pyrithione—rotate to prevent tachyphylaxis)

— Topical antifungal cream 2×/week on previously involved facial sites

— Calcineurin inhibitor maintenance (tacrolimus or pimecrolimus 2–3×/week) for chronic facial disease—steroid-sparing

— Roflumilast foam as maintenance option

— At first sign of redness or scale: increase shampoo to 3×/week, restart antifungal cream BID

— If significant inflammation: short course (5–7 days) of hydrocortisone 1–2.5% or ketoconazole + tacrolimus

— Return for visit if no improvement in 4 weeks

— Identify and avoid personal triggers (stress, alcohol, sleep deprivation)

— Gentle, fragrance-free skincare; pH-balanced cleansers

— Moderate sunlight exposure with photoprotection

— Smoking cessation

— Optimize ART in HIV patients

— Treat Parkinson disease with appropriate dopaminergic therapy

— Review medication list at every visit for SD-inducing drugs (lithium, neuroleptics)

— Chronic condition: control, not cure

— Treatment continues after clearance (maintenance) to prevent relapse

— Steroid risks: limit facial steroid use, prefer calcineurin inhibitors for maintenance

— Cost-conscious options: zinc pyrithione and selenium sulfide are OTC and effective

— Most maintenance regimens are inexpensive (OTC shampoos)

— Discourage proprietary "scalp serums" with no evidence

SD is chronic—long-term maintenance is the single most important determinant of patient satisfaction.

Maintenance pharmacotherapy:

Flare management plan (give the patient a written plan):

Lifestyle and trigger modification:

Secondary prevention of comorbid issues:

Patient education priorities:

Quality and value:

Step 3 management: At the 3-month follow-up, transition the patient from daily antifungal + steroid to antifungal shampoo 2×/week + tacrolimus ointment 2–3×/week maintenance, with a written flare action plan—classic Step 3 longitudinal care framing.

Board pearl: Stopping all therapy after clearance leads to relapse within weeks to months; counsel maintenance from the very first visit.

Follow-Up, Monitoring Parameters, and Counseling

— Initial follow-up at 4 weeks to assess response to first-line therapy

— If improving: 3-month follow-up to step down to maintenance

— If not improving: reassess diagnosis, adherence, escalate therapy, consider referral

— Stable maintenance: every 6–12 months in primary care

— Clinical: extent (BSA), erythema/scale severity, pruritus VAS, quality of life (DLQI if available)

— Adherence: ask specifically about shampoo dwell time, frequency of use, body sites treated

— Adverse effects: skin atrophy, telangiectasias, perioral dermatitis from facial steroids

— Mental health: PHQ-2 screening—visible skin disease drives depression

— Oral itraconazole/fluconazole: baseline LFTs, repeat at 4–6 weeks if continued

— ECG if QT-prolonging drug interactions

— Pregnancy test before systemic azole in women of childbearing age

— Realistic expectations: 2–4 weeks for visible improvement

— Demonstrate proper shampoo technique—lather, leave on 5 minutes, rinse

— Use shampoo on affected facial skin as a "wash" if scalp-only is insufficient

— Address stigma: SD is not contagious, not from poor hygiene

— Sleep hygiene, stress reduction (mindfulness, CBT for stress-induced flares)

— Limit alcohol, especially during flares

— Avoid hot water and harsh scrubs

Structured follow-up improves adherence and outcomes for this chronic relapsing disease.

Follow-up cadence:

What to monitor:

Lab monitoring for systemic therapy:

Counseling pearls:

Lifestyle counseling:

Vaccination and routine prevention: in HIV-positive patients identified via SD workup, ensure age-appropriate vaccines (HPV, hepatitis A/B, pneumococcal, influenza, COVID-19) and STI screening.

Step 3 management: A 35-year-old returns at 4 weeks with 50% improvement—continue current regimen another 4 weeks, reinforce maintenance plan, do not escalate prematurely; tracking response over time is the Step 3 hallmark.

Board pearl: The most common reason for "treatment failure" is inadequate shampoo dwell time (<2 minutes)—ask before changing therapy.

Ethical, Legal, and Patient Safety Considerations

— Tacrolimus/pimecrolimus carry an FDA boxed warning for theoretical malignancy risk—disclose this even though evidence is reassuring

— Document discussion of topical steroid risks (atrophy, telangiectasias, perioral dermatitis, glaucoma if near eye) before prescribing potent steroids on the face

— When severe SD prompts HIV testing, follow your state's consent rules—most allow opt-out testing; document offer and result

— Mandatory reporting of new HIV diagnoses to public health (varies by state); partner notification services should be offered

— Same-day linkage to care is best practice

— Persistent severe rash in an infant with FTT, bruising, or chronic otorrhea: rule out Langerhans cell histiocytosis and child neglect/abuse; report suspected neglect to child protective services per state law

— Verify pregnancy status before oral antifungals; fluconazole is teratogenic at high cumulative doses

— Document shared decision-making about topical use during pregnancy/lactation

— When referring to dermatology or after hospital discharge, send a written summary including prior regimens, duration, response, allergies, and current medications—incomplete handoffs are a leading source of preventable harm

— Reconcile medications at every visit—watch for lithium, interferons, EGFR inhibitors that exacerbate SD

— Patients with skin of color often have post-inflammatory hyper- or hypopigmentation that outlasts SD itself—counsel about this and avoid blaming "lack of improvement"

— Cost-conscious prescribing: OTC zinc pyrithione/selenium sulfide are evidence-based and affordable

SD touches several Step 3-flavored ethics and safety domains despite being a "benign" diagnosis.

Informed consent for off-label and steroid therapy:

HIV testing and consent:

Mandatory reporting in pediatrics:

Pregnancy and prescribing safety:

Transitions of care:

Health equity considerations:

Step 3 management: When a primary care visit uncovers HIV via SD workup, disclose the result in person, provide warm handoff to HIV clinic same day, offer partner notification, and document the conversation—this is a classic Step 3 transitions-of-care and ethics scenario.

Board pearl: Steroid phobia and steroid overuse are both safety issues—written action plans with clear "stop dates" address both.

High-Yield Associations and Rapid-Fire Clinical Facts

Malassezia (formerly Pityrosporum) species—commensal yeast central to pathogenesis; same organism causes pityriasis versicolor and Malassezia folliculitis.

HIV/AIDS prevalence of SD: 35–85%; severity inversely proportional to CD4 count.

Parkinson disease is the classic neurologic association—sebum pooling from decreased facial movement.

Drug-induced SD or SD-like eruption: lithium, interferon-α, EGFR inhibitors (cetuximab, erlotinib), buspirone, haloperidol, chlorpromazine, gold, PUVA.

Infantile cradle cap resolves by 8–12 months in nearly all cases—reassure, treat with emollient + soft brush + mild shampoo.

Petaloid distribution on presternum is highly characteristic of truncal SD.

Sebopsoriasis = overlap morphology; treat as both, refer if uncertain.

Topical roflumilast 0.3% foam is the newest FDA-approved (2023) non-steroidal option.

Oral ketoconazole is contraindicated for SD due to hepatotoxicity—use itraconazole for systemic therapy.

Tinea amiantacea: thick, asbestos-like scalp scale; reaction pattern, not specific diagnosis.

Pomade acne can mimic forehead/temple SD in patients using heavy hair products.

Photoaggravation is uncommon—most patients improve with sun exposure; photoworsening should prompt reconsidering SCLE or dermatomyositis.

Eyelid involvement: warm compresses + dilute baby shampoo lid scrubs + ketoconazole 2% cream sparingly applied to lid margin.

Selenium sulfide can discolor blonde/gray hair and silver jewelry.

Ciclopirox has both antifungal and anti-inflammatory effects—useful when both are desired.

Zinc pyrithione is OTC, inexpensive, well-tolerated for maintenance.

Smoking and alcohol independently increase SD risk and severity.

Stress and sleep deprivation are top patient-reported triggers.

Severe SD in organ transplant recipients mirrors HIV-associated patterns—optimize immunosuppression balance.

Down syndrome has increased SD prevalence.

Board pearl: "Greasy yellow scale on nasolabial folds, eyebrows, scalp, and presternum in a young man with abrupt onset"—check HIV before prescribing.

Board Question Stem Patterns

Recognize these stems—they map directly to high-yield answers.

Stem 1 — Classic adult SD: "32-year-old man with greasy yellow scale on scalp, eyebrows, and nasolabial folds for 6 months, worse in winter." → Ketoconazole 2% shampoo + ketoconazole cream; counsel chronic relapsing course.

Stem 2 — HIV trigger: "26-year-old man with sudden onset of extensive facial and chest SD plus oral thrush and 10-lb weight loss." → HIV 4th-gen Ag/Ab testing.

Stem 3 — Parkinson disease association: "72-year-old man with new facial scale, bradykinesia, rest tremor, and masked facies." → Treat SD with ketoconazole + low-potency steroid; refer to neurology for parkinsonism.

Stem 4 — Infantile cradle cap: "6-week-old with thick adherent yellow scalp scale, non-pruritic, otherwise well." → Emollient + soft brush + mild shampoo; reassure resolution by 8–12 months.

Stem 5 — Misuse of facial steroid: "Woman using clobetasol on her face for SD develops perioral pustules and erythema." → Stop steroid, start tacrolimus, add doxycycline.

Stem 6 — Drug-induced SCLE mimicking SD: "Woman on HCTZ with photodistributed facial scaly rash, positive ANA and anti-Ro." → Stop HCTZ, sun protection.

Stem 7 — Secondary infection: "Patient with SD develops honey-colored crusts on the eyebrows." → Mupirocin or oral cephalexin for impetiginization.

Stem 8 — Persistent infantile SD with red flags: "10-month-old with persistent cradle cap, hepatosplenomegaly, and purpura." → Skin biopsy for Langerhans cell histiocytosis.

Stem 9 — Refractory disease management: "Adult with SD unresponsive to 8 weeks of ketoconazole shampoo and hydrocortisone cream." → Verify adherence/dwell time first, then add tacrolimus ointment, consider oral itraconazole.

Stem 10 — Pregnancy: "28-year-old G2P1 at 20 weeks with facial SD flare." → Ketoconazole 2% shampoo + hydrocortisone 1% short course; avoid oral azoles.

Stem 11 — Sebopsoriasis: "Patient with scalp scale plus nail pitting and elbow plaques." → Treat as overlap; consider dermatology referral and PsA screening.

Step 3 management: Stems that span multiple visits typically test maintenance and follow-up—pick answers that step down to antifungal-only maintenance rather than continuing daily steroids.

Board pearl: When asked the best initial test in severe atypical SD, choose HIV testing over biopsy.

One-Line Recap

Seborrheic dermatitis is a chronic, relapsing inflammatory response to commensal Malassezia in sebum-rich skin, diagnosed clinically and managed long-term with topical antifungals as the backbone, anti-inflammatories (calcineurin inhibitors preferred over chronic steroids on face) for flares, and a low threshold to screen for HIV or Parkinson disease in severe or sudden-onset adult cases.

Diagnosis is clinical: greasy yellow scale on scalp, nasolabial folds, eyebrows, ears, presternum, and intertriginous folds; biopsy and labs only for atypia, severity, or red flags.

First-line therapy: ketoconazole 2% shampoo (5-minute dwell, 2–3×/week) + ketoconazole 2% cream BID; add short-course hydrocortisone 1–2.5% for inflammation; transition to tacrolimus 0.1% or pimecrolimus 1% for facial maintenance to avoid steroid atrophy and perioral dermatitis.

Red flags requiring workup beyond the skin: sudden/severe SD in young adult → HIV testing; new severe facial SD in older adult → evaluate for Parkinson disease; persistent infantile "cradle cap" with hepatosplenomegaly, purpura, or FTT → biopsy for Langerhans cell histiocytosis.

Longitudinal Step 3 care: counsel chronic control (not cure); maintain antifungal shampoo 1–2×/week indefinitely; written flare action plan; 4-week reassessment then 3–6-month follow-up; verify shampoo dwell time before escalating therapy; reconcile medications for SD-inducing drugs (lithium, interferons, EGFR inhibitors) at each visit.

Avoid: oral ketoconazole (hepatotoxicity), chronic potent facial steroids (atrophy, telangiectasias, perioral dermatitis), high-dose fluconazole in pregnancy (teratogenicity), and treating only the visible site while ignoring scalp reservoir.

Board pearl: Pattern recognition—greasy yellow scale + sebum-rich distribution + chronic relapse = seborrheic dermatitis; always ask "why now, why severe?" to catch HIV, Parkinson disease, and drug triggers.