Kligman's Picture of The Stages Of Rosacea

Stages - Plewig and Kligman Classification of Rosacea

(Taken from their book, Acne and Rosacea, Second Edition, 1993)

Stage I: The erythema (redness) may persist for hours and days, hence the old term erthema congestivum (redness congestion). Erythema lasting only a few minutes is not early rosacea. Telangiectases becomes progressively prominent, forming sprays on the nose, nasolabial folds, checks, and glabella. Most of these patients complain of sensitive skin that stings, burns, and itches after application of a variety of cosmetics, especially certain fragrances and sunscreens. Trauma from abrasives and peeling agents readily induces long-lasting erythema, thus the facial skin is unusually vulnerable to chemical and physical stimuli.

Stage II: Inflammatory papules and pustules crop up and persist for weeks. Some papules show a small pustule at the apex, justifying the term papulopustular. The lesions are always follicular in origin, mainly in sebaceous follicles but also in the smaller and more numerous vellus follicles. Comedones do not occur. The deeper inflammatory lesions may heal with scarring, but scars are inconspicuous and tend to be shallow. Facial pores become larger and prominent. If there has been much solar exposure over decades, the stigmata of photodamaged skin becomes superimposed, namely yellowed, leathered skin (elastosis), wrinkles and solar comedones. The papulopustular attacks become more and more frequent. Finally, rosacea may extend over the entire face and even spread to the scalp, especially if the patient is balding. Itchy follicular pustules of the scalp are typical. Eventually, the sides of the neck as well as the retroauricular and presternal area may be affected.

Stage III: A small proportion of patients develop more serious expressions of the disease, namely large inflammatory nodules, furunculoid infiltrations, and tissue hyperplasia. These derangements occur particularly on the cheeks and nose, less often on the chin, forehead, or ears. The facial contours gradually become coarse, thickened, and irregular. Curiously, patients may not notice these disfigurements. The deranged appearance becomes evident when photographs from previous years are reviewed. Finally, the patient shows diffusely inflamed, thickened, edematous skin with large pores, resembling the peel of an orange. These coarse features are due to extensively inflammatory infiltration, connective tissue hypertrophy, massive fibrosis and elastosis, diffuse sebaceous gland hyperplasia, and extreme enlargement of individual sebaceous glands forming dozens of yellowish unbilicated papules on the cheeks, forehead, temples, and nose. Thickened folds and ridges may create a grotesque appearance mimicking leonine facies of leprosy or leukemia. The ultimate deformity is the phymas, of which rhinophyma is the prototype.