DermatologyTier 1Disease (DEADMAN)

Rosacea

Description

Chronic inflammatory facial dermatosis - centrofacial (cheeks, nose, chin, forehead), spares periocular skin
Classified by phenotype rather than rigid subtype (modern approach) - patients often have overlapping features:
- Erythematotelangiectatic - persistent central facial erythema, flushing, telangiectasia
- Papulopustular - inflammatory papules/pustules, no comedones (key discriminator from acne)
- Phymatous - skin thickening, sebaceous hyperplasia, classically rhinophyma (nose)
- Ocular rosacea - blepharitis, conjunctivitis, dry/gritty eyes - can precede skin signs

Onset typically 30-50 years; F>M overall, but rhinophyma disproportionately affects men
More common in fair-skinned (Fitzpatrick I-II) populations of Celtic/Northern European descent

Multifactorial: neurovascular dysregulation (abnormal flushing response), innate immune dysregulation (cathelicidin/LL-37 overactivity), Demodex folliculorum mite overgrowth implicated in papulopustular disease
Triggers (vasodilation/flare): heat, sun exposure (UV), alcohol, spicy food, hot drinks, stress, exercise - identifying and avoiding individual triggers is a core part of management
Not a disorder of sebum production (contrast with acne) and not infective in the primary sense, despite Demodex association

Clinical - diagnosis by phenotype pattern

Centrofacial erythema/flushing/telangiectasia +/- papulopustular lesions without comedones
Ask specifically about ocular symptoms (dryness, grittiness, blepharitis) - often underreported

Differential

	Discriminator
Acne vulgaris	Comedones present, not confined to central face flushing pattern
Seborrhoeic dermatitis	Greasy scale, nasolabial folds, can coexist
Systemic lupus erythematosus (malar rash)	Spares nasolabial folds (rosacea does not spare them as sharply), photosensitive, other SLE features
Perioral dermatitis	Perioral/periocular papules, often from topical steroid use

A. All patients - foundational

Trigger avoidance (sun, heat, alcohol, spicy food), daily broad-spectrum sunscreen, gentle skincare, avoid topical corticosteroids on the face (can worsen/precipitate rosacea)

B. Papulopustular disease

Topical metronidazole, azelaic acid, or ivermectin cream - first-line
Oral doxycycline (low, anti-inflammatory sub-antimicrobial dose) for moderate-severe disease - anti-inflammatory effect, not primarily antibacterial
Oral isotretinoin (low dose) for severe/refractory disease

C. Erythema/flushing/telangiectasia

Topical brimonidine or oxymetazoline (alpha-agonist vasoconstrictors) - reduce background erythema for hours, do not treat inflammatory lesions
Vascular laser/IPL - effective for persistent telangiectasia and background erythema, not first-line/subsidised universally

D. Phymatous change

Early: oral isotretinoin may limit progression
Established rhinophyma - surgical/laser debulking (ablative laser, shave excision) - medical therapy does not reverse established phymatous change

E. Ocular rosacea

Lid hygiene, artificial tears; oral doxycycline for more significant disease; ophthalmology referral if severe/vision-threatening

Ocular disease (blepharitis, dry eye, keratitis)
Migraine, cardiovascular disease - reported epidemiological associations with rosacea severity
Anxiety/depression - facial visibility drives significant psychosocial burden
Fair skin/UV-damaged skin phenotype

Chronic, relapsing-remitting course over years to decades; triggers drive individual flares
Untreated papulopustular/phymatous disease can progress to permanent skin thickening (rhinophyma) - not reversible with medical therapy once established
Ocular involvement can threaten vision if severe/untreated (keratitis)
Generally responds well to a trigger-avoidance plus topical/oral regimen, but recurrence is the rule if therapy is stopped

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