Epidemiology
Rosacea in childhood is most likely underreported because of its clinical similarity to other erythematous facial disorders.1 Rosacea is generally thought of as a disease of fair-skinned, young to middle-aged adults, though it has been noted to affect people of other complexions and ages.2 Most full-blown cases in the pediatric population have been in light-skinned children ranging from infants to adolescents.
Etiology
The etiology of rosacea is unknown, though certain exacerbating factors undoubtedly have a role in predisposed individuals.3,4 Emotions such as anger, anxiety, and embarrassment can lead to flushing. Environmental conditions such as wind, cold, humidity, or heat from any source (eg, sun, sauna, whirlpool, vigorous exercise) can do the same. Vasodilators such as alcohol or vasodilatory medications can lead to flushing, though these are not likely causes in children. Spicy foods such as chili, curry, and peppers, as well as hot foods and beverages including coffee, tea, and hot chocolate, may contribute to symptoms. Irritants such as alcohol-based cleansers, astringents, perfume, shaving lotion, certain soaps, sunscreen, and facecloths may aggravate rosacea.3,4 Saprophytic mites (Demodex folliculorum and Demodex brevis) may cause an inflammatory or allergic reaction by either blocking hair follicles or acting as vectors for microorganisms that some believe may be responsible for or may trigger rosacea.5 Immunodeficiency, as in patients with human immunodeficiency virus, also may contribute to the development of rosacea.6
Genetics plays an uncertain role in the development of blushing and ultimately rosacea. If vasodilator substances or mediators are implicated in the development of rosacea as postulated, the disease may have a genetic basis because such mediators are often under the control of single genes.7 In one study, 20% of children with rosacea were found to have a history of rosacea in their immediate families, though this number may be an underestimate because only one parent of each patient was examined and half of the parents clinically diagnosed with rosacea reported no familial involvement.8 A family history of perioral dermatitis also may be important, as this condition may be related to rosacea.9
Pathophysiology
Chronic transient vasodilation, as occurs with blushing, is the earliest representation of rosacea. The warmth and redness associated with flushing is caused by vasodilation, allowing excess blood flow, and by engorgement of the subpapillary venous plexus.2 Flushing without sweating is typically seen in children and is likely due to circulating vasodilator substances or mediators such as bradykinin, catecholamines, cytokines, endorphins, gastrin, histamine, neuropeptides, serotonin, substance P, and vascular endothelial growth factor.10 A flaw in the autonomic innervation of the cutaneous vasculature also is a likely mechanism.10
Clinical Description
The first stage of rosacea consists of blushing, in which the face becomes bright red in response to certain stimuli (Figure). Episodes of erythema are recurrent and last longer than normal physiologic flushing, which typically subsides within minutes.11 Telangiectasias can become apparent over time. Children in this early stage of the condition may complain of burning or irritation.
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In the second, or intermediate, stage of rosacea, the rash consists of papules and pustules on a background of erythema with telangiectasias confined to the child's face. Although peripheral involvement of the back, upper chest, and scalp may be seen in adults, these areas seem to be spared in the pediatric population.12
The third, or late, stage of rosacea involves coarse skin, inflammatory nodules, or gross enlargement of facial features.11 Such chronic changes do not occur in children as they do in adults, presumably because the disease process takes more time to evolve.13
Eye involvement can occur in children.14 It may include manifestations such as blepharoconjunctivitis, episcleritis, keratitis, meibomianitis, chalazia, hordeola, and hyperemic conjunctivae.15,16 Although any of these eye conditions can potentially occur in children, meibomian gland inflammation and keratitis are the common findings noted.17 Peripheral vascularization followed by subepithelial infiltrates can lead to scarring or perforation in the lower two thirds of the cornea. The disease may be unilateral, but most commonly it affects both eyes.17
Steroid-induced rosacea also has been termed iatrosacea because of its mode of acquisition.18 Topical fluorinated and low-dose corticosteroids can cause a rosacealike dermatitis of the face consisting of persistent erythema with papules, pustules, telangiectasias, and sometimes atrophy.19-22 Corticosteroids may be an exacerbating factor leading to classic rosacea rather than the cause of an independent disease.2 The distribution of steroid rosacea to the eyelids and lateral face may help distinguish it from the centrally located typical rosacea.23 A case of pediatric rosacea associated with the use of topical fluorinated glucocorticosteroids was identified in a 9-month-old boy and 16-year-old girl, both with erythematous patches and papules on the cheeks, paranasal areas, and chin.18,23 Forty-six boys and 60 girls, ranging in age of onset from 6 months to 13 years (average, 7 years), were diagnosed with steroid rosacea. Nearly all of the children had perinasal and perioral involvement of erythematous skin interspersed with papules and/or pustules. The lower eyelids were affected in roughly half of the patients.8