Nicole L. Lacz, MD

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.

Please refer to the PDF to view the figure

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 

Diagnosis

Consistent flushing in children may be a sign of vasomotor instability and early rosacea. These children may blush more frequently and with greater intensity for longer periods than their peers exposed to the same stimuli.²⁴ Thus, blushing in the early stage of rosacea may be an accentuation of the body's normal physiologic response system. A diagnosis of pediatric rosacea beyond the initial stage should be considered when a healthy child has acuminate papules and small pustules of the face, especially if there also exists flushing, telangiectasias, or a family history of rosacea.¹⁴ 

Differential Diagnosis

The earliest form of rosacea, facial blushing, may be difficult to distinguish from flushing due to other causes. Blushing due to emotions such as embarrassment or anger and to exercise-induced flushing are both appropriate reactions to such stimuli, whereas blushing in the first stage of rosacea may be an exaggeration of this phenomenon.² The main pathway for thermoregulatory and emotional flushing is the cervical sympathetic outflow tract.²⁵ Gustatory blushing, as occurs with consumption of spicy foods, is mediated by autonomic neurons via a branch of the trigeminal nerve.² Sweating often occurs in conjunction with the aforementioned causes of flushing, but it is rarely associated with rosacea flushing. Thus, sweating may be helpful in reaching a diagnosis; however, exceptions exist.² Frey syndrome (auriculotemporal syndrome), which is characterized by warmth and sweating in the malar region caused by aberrant autonomic fiber connections after damage in the parotid region, may mimic the early stage of rosacea.

The intermediate stage of pediatric rosacea may be confused with other papulopustular disorders such as acne vulgaris, perioral dermatitis, and lupus erythematosus (Table). Careful attention to symptoms, distribution of facial lesions, and potential biopsy results are warranted to distinguish between the conditions. Steroid rosacea and perioral dermatitis may be variants of rosacea or completely separate conditions.^9,26

Please refer to the PDF to view the table

Perioral dermatitis is a rosacealike dermatitis characterized by erythematous papules and pustules usually confined to the perioral region, though the perinasal and periocular areas may be involved.²⁷ A granulomatous perioral dermatitis with tiny, closely spaced, flesh-colored papules in the perioral, perinasal, and periorbital areas was described in children aged 3 to 11 years.²⁸ All cases had spontaneous resolution of symptoms regardless of treatment. The patients did not exhibit flushing or telangiectasias.²⁸

The classic butterfly rash, consisting of erythema and telangiectasia of the malar region and associated with systemic lupus erythematosus, also can be confused with rosacea. Histopathologic examination and direct immunofluorescence of the lesion may help to differentiate lupus from rosacea.¹⁴ 

Laboratory Diagnosis

There is no specific histologic change unique to rosacea.¹² The most common findings are telangiectasia, edema, elastosis, a variable amount of superficial and deep perivascular lymphohistiocytic inflammatory infiltrate loosely arranged around the hair follicles, and especially architectural disruption of the upper dermis.^12,28 Depending on the variant of rosacea, there may be an exaggeration of one or more histopathologic signs.¹² For example, granulomatous rosacea may contain collections of granulomas with multinucleated giant cells.²⁸

Treatment

Treatment is gradual and largely determined by the clinical type of rosacea. Children with early or intermediate stages of rosacea are encouraged to avoid their individual local triggers to prevent flares. Topical corticosteroids, especially fluorinated medications, should be discouraged, because even low-potency steroids, including over-the-counter preparations and hydrocortisone 1%, have been shown to cause worsening of the condition.⁸

Traditional therapy for rosacea includes topical and systemic antibiotics, topical metronidazole, and topical retinoids. Oral tetracycline can be used for adolescents in doses similar to those prescribed for adults. It should not be used in children younger than approximately 9 years¹⁷ because it is known to cause dental staining and to be deposited in the skeletal system where it can cause temporary depression in bone growth.^29,30 Azithromycin or a low dose of doxycycline can be used with good results.^31,32 For younger children, oral erythromycin is safe and effective to eliminate the erythema, papules, and pustules of rosacea.³² Topical erythromycin and clindamycin have been used with varying results. Azelaic acid and isotretinoin also may be effective.³³ Topical metronidazole 0.75% gel has proven effective in clinical trials.^34,35 A combination of systemic antibiotics and topical treatment may lead to a substantial reduction in inflammatory lesions, erythema, and the size and diameter of telangiectatic vessels.³²

Eyelid hygiene and erythromycin or bacitracin ointment, to improve meibomian gland function, are appropriate initial treatments for the ocular manifestations of childhood rosacea.^17,36 A low dose of steroid drops can manage significant irritation when needed. Systemic therapy with tetracycline or other oral pharmaceuticals used to treat the face also may work for ocular symptoms.¹⁷

The treatment of steroid rosacea is a slow process often involving antiacne agents such as benzoyl peroxide and oral or topical antibiotics.²³ Abrupt discontinuation of topical steroids followed by administration of antibiotics is a suitable treatment option. Prior recommendation has been to taper all topical steroids to prevent rebound flare; however, one study found clearing of symptoms by week 3 in 22% of patients, by week 4 in 86% of patients, and by week 8 in 100% of patients following abrupt cessation of topical steroids and a regimen of oral erythromycin stearate or topical clindamycin phosphate in children with erythromycin allergy or intolerance.⁸ Thus, a gradual withdrawal of topical nonfluorinated steroids may not be necessary. However, it is more common than not for children to experience an initial flare of their condition upon withdrawal from topical fluorinated steroids. This is followed by a slow and steady fading.²³ 

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.

Please refer to the PDF to view the figure

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 

Diagnosis

Consistent flushing in children may be a sign of vasomotor instability and early rosacea. These children may blush more frequently and with greater intensity for longer periods than their peers exposed to the same stimuli.²⁴ Thus, blushing in the early stage of rosacea may be an accentuation of the body's normal physiologic response system. A diagnosis of pediatric rosacea beyond the initial stage should be considered when a healthy child has acuminate papules and small pustules of the face, especially if there also exists flushing, telangiectasias, or a family history of rosacea.¹⁴ 

Differential Diagnosis

The earliest form of rosacea, facial blushing, may be difficult to distinguish from flushing due to other causes. Blushing due to emotions such as embarrassment or anger and to exercise-induced flushing are both appropriate reactions to such stimuli, whereas blushing in the first stage of rosacea may be an exaggeration of this phenomenon.² The main pathway for thermoregulatory and emotional flushing is the cervical sympathetic outflow tract.²⁵ Gustatory blushing, as occurs with consumption of spicy foods, is mediated by autonomic neurons via a branch of the trigeminal nerve.² Sweating often occurs in conjunction with the aforementioned causes of flushing, but it is rarely associated with rosacea flushing. Thus, sweating may be helpful in reaching a diagnosis; however, exceptions exist.² Frey syndrome (auriculotemporal syndrome), which is characterized by warmth and sweating in the malar region caused by aberrant autonomic fiber connections after damage in the parotid region, may mimic the early stage of rosacea.

The intermediate stage of pediatric rosacea may be confused with other papulopustular disorders such as acne vulgaris, perioral dermatitis, and lupus erythematosus (Table). Careful attention to symptoms, distribution of facial lesions, and potential biopsy results are warranted to distinguish between the conditions. Steroid rosacea and perioral dermatitis may be variants of rosacea or completely separate conditions.^9,26

Please refer to the PDF to view the table

Perioral dermatitis is a rosacealike dermatitis characterized by erythematous papules and pustules usually confined to the perioral region, though the perinasal and periocular areas may be involved.²⁷ A granulomatous perioral dermatitis with tiny, closely spaced, flesh-colored papules in the perioral, perinasal, and periorbital areas was described in children aged 3 to 11 years.²⁸ All cases had spontaneous resolution of symptoms regardless of treatment. The patients did not exhibit flushing or telangiectasias.²⁸

The classic butterfly rash, consisting of erythema and telangiectasia of the malar region and associated with systemic lupus erythematosus, also can be confused with rosacea. Histopathologic examination and direct immunofluorescence of the lesion may help to differentiate lupus from rosacea.¹⁴ 

Laboratory Diagnosis

There is no specific histologic change unique to rosacea.¹² The most common findings are telangiectasia, edema, elastosis, a variable amount of superficial and deep perivascular lymphohistiocytic inflammatory infiltrate loosely arranged around the hair follicles, and especially architectural disruption of the upper dermis.^12,28 Depending on the variant of rosacea, there may be an exaggeration of one or more histopathologic signs.¹² For example, granulomatous rosacea may contain collections of granulomas with multinucleated giant cells.²⁸

Treatment

Treatment is gradual and largely determined by the clinical type of rosacea. Children with early or intermediate stages of rosacea are encouraged to avoid their individual local triggers to prevent flares. Topical corticosteroids, especially fluorinated medications, should be discouraged, because even low-potency steroids, including over-the-counter preparations and hydrocortisone 1%, have been shown to cause worsening of the condition.⁸

Traditional therapy for rosacea includes topical and systemic antibiotics, topical metronidazole, and topical retinoids. Oral tetracycline can be used for adolescents in doses similar to those prescribed for adults. It should not be used in children younger than approximately 9 years¹⁷ because it is known to cause dental staining and to be deposited in the skeletal system where it can cause temporary depression in bone growth.^29,30 Azithromycin or a low dose of doxycycline can be used with good results.^31,32 For younger children, oral erythromycin is safe and effective to eliminate the erythema, papules, and pustules of rosacea.³² Topical erythromycin and clindamycin have been used with varying results. Azelaic acid and isotretinoin also may be effective.³³ Topical metronidazole 0.75% gel has proven effective in clinical trials.^34,35 A combination of systemic antibiotics and topical treatment may lead to a substantial reduction in inflammatory lesions, erythema, and the size and diameter of telangiectatic vessels.³²

Eyelid hygiene and erythromycin or bacitracin ointment, to improve meibomian gland function, are appropriate initial treatments for the ocular manifestations of childhood rosacea.^17,36 A low dose of steroid drops can manage significant irritation when needed. Systemic therapy with tetracycline or other oral pharmaceuticals used to treat the face also may work for ocular symptoms.¹⁷

The treatment of steroid rosacea is a slow process often involving antiacne agents such as benzoyl peroxide and oral or topical antibiotics.²³ Abrupt discontinuation of topical steroids followed by administration of antibiotics is a suitable treatment option. Prior recommendation has been to taper all topical steroids to prevent rebound flare; however, one study found clearing of symptoms by week 3 in 22% of patients, by week 4 in 86% of patients, and by week 8 in 100% of patients following abrupt cessation of topical steroids and a regimen of oral erythromycin stearate or topical clindamycin phosphate in children with erythromycin allergy or intolerance.⁸ Thus, a gradual withdrawal of topical nonfluorinated steroids may not be necessary. However, it is more common than not for children to experience an initial flare of their condition upon withdrawal from topical fluorinated steroids. This is followed by a slow and steady fading.²³ 

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.

Please refer to the PDF to view the figure

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 

Diagnosis

Consistent flushing in children may be a sign of vasomotor instability and early rosacea. These children may blush more frequently and with greater intensity for longer periods than their peers exposed to the same stimuli.²⁴ Thus, blushing in the early stage of rosacea may be an accentuation of the body's normal physiologic response system. A diagnosis of pediatric rosacea beyond the initial stage should be considered when a healthy child has acuminate papules and small pustules of the face, especially if there also exists flushing, telangiectasias, or a family history of rosacea.¹⁴ 

Differential Diagnosis

The earliest form of rosacea, facial blushing, may be difficult to distinguish from flushing due to other causes. Blushing due to emotions such as embarrassment or anger and to exercise-induced flushing are both appropriate reactions to such stimuli, whereas blushing in the first stage of rosacea may be an exaggeration of this phenomenon.² The main pathway for thermoregulatory and emotional flushing is the cervical sympathetic outflow tract.²⁵ Gustatory blushing, as occurs with consumption of spicy foods, is mediated by autonomic neurons via a branch of the trigeminal nerve.² Sweating often occurs in conjunction with the aforementioned causes of flushing, but it is rarely associated with rosacea flushing. Thus, sweating may be helpful in reaching a diagnosis; however, exceptions exist.² Frey syndrome (auriculotemporal syndrome), which is characterized by warmth and sweating in the malar region caused by aberrant autonomic fiber connections after damage in the parotid region, may mimic the early stage of rosacea.

The intermediate stage of pediatric rosacea may be confused with other papulopustular disorders such as acne vulgaris, perioral dermatitis, and lupus erythematosus (Table). Careful attention to symptoms, distribution of facial lesions, and potential biopsy results are warranted to distinguish between the conditions. Steroid rosacea and perioral dermatitis may be variants of rosacea or completely separate conditions.^9,26

Please refer to the PDF to view the table

Perioral dermatitis is a rosacealike dermatitis characterized by erythematous papules and pustules usually confined to the perioral region, though the perinasal and periocular areas may be involved.²⁷ A granulomatous perioral dermatitis with tiny, closely spaced, flesh-colored papules in the perioral, perinasal, and periorbital areas was described in children aged 3 to 11 years.²⁸ All cases had spontaneous resolution of symptoms regardless of treatment. The patients did not exhibit flushing or telangiectasias.²⁸

The classic butterfly rash, consisting of erythema and telangiectasia of the malar region and associated with systemic lupus erythematosus, also can be confused with rosacea. Histopathologic examination and direct immunofluorescence of the lesion may help to differentiate lupus from rosacea.¹⁴ 

Laboratory Diagnosis

There is no specific histologic change unique to rosacea.¹² The most common findings are telangiectasia, edema, elastosis, a variable amount of superficial and deep perivascular lymphohistiocytic inflammatory infiltrate loosely arranged around the hair follicles, and especially architectural disruption of the upper dermis.^12,28 Depending on the variant of rosacea, there may be an exaggeration of one or more histopathologic signs.¹² For example, granulomatous rosacea may contain collections of granulomas with multinucleated giant cells.²⁸

Treatment

Treatment is gradual and largely determined by the clinical type of rosacea. Children with early or intermediate stages of rosacea are encouraged to avoid their individual local triggers to prevent flares. Topical corticosteroids, especially fluorinated medications, should be discouraged, because even low-potency steroids, including over-the-counter preparations and hydrocortisone 1%, have been shown to cause worsening of the condition.⁸

Traditional therapy for rosacea includes topical and systemic antibiotics, topical metronidazole, and topical retinoids. Oral tetracycline can be used for adolescents in doses similar to those prescribed for adults. It should not be used in children younger than approximately 9 years¹⁷ because it is known to cause dental staining and to be deposited in the skeletal system where it can cause temporary depression in bone growth.^29,30 Azithromycin or a low dose of doxycycline can be used with good results.^31,32 For younger children, oral erythromycin is safe and effective to eliminate the erythema, papules, and pustules of rosacea.³² Topical erythromycin and clindamycin have been used with varying results. Azelaic acid and isotretinoin also may be effective.³³ Topical metronidazole 0.75% gel has proven effective in clinical trials.^34,35 A combination of systemic antibiotics and topical treatment may lead to a substantial reduction in inflammatory lesions, erythema, and the size and diameter of telangiectatic vessels.³²

Eyelid hygiene and erythromycin or bacitracin ointment, to improve meibomian gland function, are appropriate initial treatments for the ocular manifestations of childhood rosacea.^17,36 A low dose of steroid drops can manage significant irritation when needed. Systemic therapy with tetracycline or other oral pharmaceuticals used to treat the face also may work for ocular symptoms.¹⁷

The treatment of steroid rosacea is a slow process often involving antiacne agents such as benzoyl peroxide and oral or topical antibiotics.²³ Abrupt discontinuation of topical steroids followed by administration of antibiotics is a suitable treatment option. Prior recommendation has been to taper all topical steroids to prevent rebound flare; however, one study found clearing of symptoms by week 3 in 22% of patients, by week 4 in 86% of patients, and by week 8 in 100% of patients following abrupt cessation of topical steroids and a regimen of oral erythromycin stearate or topical clindamycin phosphate in children with erythromycin allergy or intolerance.⁸ Thus, a gradual withdrawal of topical nonfluorinated steroids may not be necessary. However, it is more common than not for children to experience an initial flare of their condition upon withdrawal from topical fluorinated steroids. This is followed by a slow and steady fading.²³