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Approach to the patient with facial erythema

Author Section Editor Deputy Editor


Mark V Dahl, MD Erik Stratman, MD Abena O Ofori, MD

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Nov 2017. | This topic last updated: Aug 12, 2016.
INTRODUCTION — Facial erythema (facial redness), a clinical finding most noticeable in fair-skinned individuals, occurs as a result of cutaneous blood vessel dilation and increased
blood flow to the skin. Although transient facial erythema is often observed as a normal, neurologically-mediated response to strong emotion, exercise, or heat exposure, inflammation and
a variety of medical conditions can lead to longer-lasting and symptomatic or cosmetically distressing facial erythema.

Examples of disorders that may present with diffuse or localized facial erythema and the evaluation of patients with this clinical finding will be reviewed here. More detailed information on
flushing and many of the other disorders associated with facial erythema is available separately. (See "Approach to flushing in adults" and 'Etiology' below.)

ETIOLOGY — A variety of factors, including primary skin diseases, external insults, and systemic illness may cause facial redness. Knowledge of the distinctive characteristics of these
disorders is helpful for diagnosis.

Primary inflammatory skin diseases

● Rosacea – The erythematotelangiectatic subtype of rosacea is characterized by centrofacial erythema and telangiectasias (picture 1A-B) [1]. Affected patients also often exhibit
flushing and sensitivity of facial skin. The patient history and physical findings are usually sufficient for the diagnosis of this disorder. Other rosacea subtypes may also demonstrate
these clinical features. (See "Rosacea: Pathogenesis, clinical features, and diagnosis".)

● Perioral dermatitis – Perioral dermatitis (also known as periorificial dermatitis) presents with multiple, small, inflammatory papules clustered around the mouth, nose, or eyes
(picture 2). Fine scale and dermatitis are also often present, but the rash is characteristically more red and bumpy than red and scaly. In patients with perioral lesions, the skin
immediately adjacent to the vermillion border of the lip is classically spared. Perioral dermatitis most frequently affects young women; occasionally the disorder occurs in children.
(See "Perioral (periorificial) dermatitis".)

● Seborrheic dermatitis – Erythema accompanied by greasy yellow-white scale is a characteristic feature of seborrheic dermatitis in adults. In patients with dark skin, the scale may
have a gray or brown hue. Involvement of the face typically manifests in the nasolabial folds, eyebrows, glabella, and lateral nasal areas (picture 3A-B). Other potential sites of
involvement include the scalp, ears, chest, axillae, and groin. The diagnosis of seborrheic dermatitis is usually made based upon the clinical findings [2]. (See "Seborrheic dermatitis
in adolescents and adults".)

● Atopic dermatitis – Facial involvement of atopic dermatitis is common in infants (picture 4A-C), but may also occur in older children and adults (picture 5A-B). Intensely pruritic
erythematous patches or plaques with accompanying scale, exudate, excoriations, or lichenification are often seen. The presence of a chronic, very pruritic, dermatitic skin disorder
with lichenification in a typical distribution suggests the possibility of atopic dermatitis [3]. Patients may also exhibit an extra skin fold beneath the bilateral lower eyelids that is known
as a Dennie-Morgan fold (picture 6). (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis".)

● Psoriasis – The clinical findings in facial psoriasis may be more subtle than the classic thick plaques with silver scale that are typical of lesions in other body areas (picture 7A-B). In
some patients, lesions closely resemble the erythematous patches and finer scale of seborrheic dermatitis. The detection of lesions consistent with the classic presentation of
psoriasis elsewhere on the body is helpful for diagnosis. (See "Epidemiology, clinical manifestations, and diagnosis of psoriasis".)

Disorders due to external insults

● Irritant contact dermatitis – Contact with skin care products, cosmetics, or other substances that contain irritants may result in facial eruptions with features of eczematous
dermatitis. The dermatitis may be diffuse or localized depending on the sites of contact. The facial folds and the delicate skin of the eyelids are particularly susceptible to more severe
involvement.

Unlike allergic contact dermatitis, which is typically associated with intense pruritus, patients with irritant contact dermatitis tend to complain of burning or prickling sensations [4]. The
patient history is critical for identifying this diagnosis. (See "Irritant contact dermatitis in adults".)

● Allergic contact dermatitis – Delayed hypersensitivity reactions to external substances that contact the skin can cause acute, intense inflammatory reactions characterized by
bright erythema, scale, and exudate (picture 8A-B) [4]. Other times, the dermatitis is only mildly inflamed and chronic. Patch testing can be useful for identifying the causative
antigenic substance. (See "Clinical features and diagnosis of allergic contact dermatitis" and "Patch testing".)

Photosensitive disorders

● Sunburn – The appearance of confluent, erythematous patches following sun exposure is a classic feature of sunburn. Pruritus or pain may also be present. In severe cases, edema
and blistering can occur. Desquamation commonly occurs during healing. (See "Sunburn".)

● Polymorphous light eruption (PMLE) – Often colloquially referred to as sun poisoning or sun allergy, PMLE may present with a wide variety of clinical manifestations [5].
Erythematous patches, papules, vesicles, or plaques may occur within hours to days after sun exposure (picture 9). PMLE is particularly likely to occur in early spring, as patient
tolerance to sunlight tends to rise with increasing exposure. (See "Polymorphous light eruption".)

● Phototoxic and photoallergic eruptions – Phototoxic eruptions are sunburn-like reactions induced by the ingestion or application of photosensitizing substances (picture 10) [6-8].
The photosensitizing agent decreases the amount of ultraviolet light exposure required to elicit this reaction. Severe eruptions with blistering and edema may occur. (See
"Photosensitivity disorders (photodermatoses): Clinical manifestations, diagnosis, and treatment", section on 'Phototoxicity'.)

Photoallergic reactions are characterized by pruritic, eczematous eruptions in sun exposed areas (picture 11) [6-8]. Topical, rather than ingested, agents are the most frequent
causes of photoallergic reactions [9]. (See "Photosensitivity disorders (photodermatoses): Clinical manifestations, diagnosis, and treatment", section on 'Photoallergy'.)

● Photodamage – The formation of numerous telangiectasias and a ruddy complexion secondary to chronic sun exposure is a common cause of facial redness [10]. Sun protected
areas of the face are relatively spared. Patients may have accompanying poikiloderma of Civatte, a disorder characterized by mottled pigmentation and telangiectasias on the lateral
neck (picture 12). (See "Photoaging", section on 'Clinical features'.)

● Acute cutaneous lupus erythematosus, dermatomyositis, and lupus tumidus erythematosus [11]. (See 'Systemic disorders' below and 'Localized inflammatory infiltrates'
below.)

Systemic disorders

● Acute cutaneous lupus erythematosus – Patients with systemic lupus erythematosus may develop acute cutaneous lupus erythematosus, which often manifests as persistent
violaceous erythema on the malar area of the face (picture 13) [12]. This clinical finding is often referred to as a “butterfly rash.” The prominent telangiectasias of rosacea are not a
feature of acute cutaneous lupus erythematosus. The presence of signs or symptoms of systemic lupus erythematosus suggests this diagnosis. (See "Overview of cutaneous lupus
erythematosus", section on 'Acute cutaneous lupus erythematosus' and "Overview of the clinical manifestations of systemic lupus erythematosus in adults" and "Systemic lupus
erythematosus (SLE) in children: Clinical manifestations and diagnosis".)

● Dermatomyositis – A classic sign of dermatomyositis is the “heliotrope eruption,” a violaceous and often edematous eruption that occurs on the eyelids and periorbital skin (picture
14A-B) [13]. Patients may or may not have accompanying proximal muscle weakness. The detection of other cutaneous signs of dermatomyositis, such as Gottron papules and
periungual telangiectasias raise suspicion for this diagnosis. In addition, the possibility of an underlying malignancy must be considered in adults with dermatomyositis. (See "Clinical
manifestations of dermatomyositis and polymyositis in adults" and "Juvenile dermatomyositis and polymyositis: Epidemiology, pathogenesis, and clinical manifestations".)

Infectious disorders

● Viral infections – Erythema infectiosum is a viral disease caused by parvovirus B19 that most commonly occurs in children [14]. A common feature of this disorder is the
appearance of red patches on the cheeks that resemble facial skin after a slap on the face (picture 15). Nonspecific constitutional symptoms, such as fever, coryza, headache, or
gastrointestinal distress usually precede the cutaneous findings. A reticulated eruption on the trunk and extremities frequently appears one to two days after the facial lesions. (See
"Clinical manifestations and diagnosis of parvovirus B19 infection", section on 'Erythema infectiosum'.)

Morbilliform or confluent facial redness may also occur as early features of other viral infections such as measles or rubella; other body sites are typically also involved (picture 16A-
B). (See "Measles: Clinical manifestations, diagnosis, treatment, and prevention" and "Rubella".)

● Erysipelas – Erysipelas is a superficial form of cellulitis that usually results from infection with beta-hemolytic streptococci [15]. Patients typically present with the acute development
of an erythematous, warm, edematous, and well-defined plaque (picture 17). Fever and lymphadenopathy often accompany the cutaneous symptoms. (See "Cellulitis and skin
abscess: Clinical manifestations and diagnosis".)

Localized inflammatory infiltrates

● Lupus tumidus erythematosus – Also known as tumid lupus erythematosus, lupus tumidus erythematosus is an uncommon disorder that presents with erythematous plaques in
sun-exposed areas such as the face, neck, upper trunk, and upper extremities and scale is typically absent (picture 18) [16,17]. The vast majority of patients do not have associated
systemic lupus. The performance of a biopsy assists with diagnosis. (See "Overview of cutaneous lupus erythematosus", section on 'Lupus erythematosus tumidus'.)

● Jessner’s lymphocytic infiltrate – This idiopathic disorder most commonly manifests as erythematous, asymptomatic, often annular plaques on the face, neck, or upper trunk
(picture 19A-B) [18,19]. A skin biopsy is useful for diagnosis. Jessner’s lymphocytic infiltrate shares clinical and histopathological features with lupus tumidus erythematous. The
relationship between these disorders remains unclear [19].

● Granuloma faciale – Granuloma faciale usually presents as a solitary, red-brown, asymptomatic, round plaque with follicular prominence on the face (picture 20) [20]. The
histopathologic finding of a normal-appearing thin zone in the papillary dermis (Grenz zone) above a dense inflammatory dermal infiltrate containing eosinophils, lymphocytes,
neutrophils, and plasma cells is characteristic of this diagnosis. The disorder is most common in Caucasian men [20]. (See "Granuloma faciale".)

● Cutaneous lymphoid hyperplasia (lymphocytoma cutis) – Cutaneous lymphoid hyperplasia occurs as a result of antigenic stimulation in the skin leading to lymphocyte
proliferation. The specific cause of the disorder is often unknown, but insect bites and infections, including Lyme disease, have been linked to some cases [21,22]. Patients typically
present with a red-brown to violaceous nodule or plaque. A skin biopsy is necessary for diagnosis. (See "Clinical manifestations of Lyme disease in adults", section on 'Borrelial
lymphocytoma'.)

● Tinea faciei – Infections with dermatophytic fungi can mimic other acute and chronic facial skin diseases depending upon the nature of the infecting organism and the intensity of the
host’s defense reaction. In general, facial fungal infections tend to be unilateral; sharply marginated; occasionally annular, scaling, or weeping; and slowly enlarging plaques (picture
21). Potassium hydroxide examination of scale or culture confirms the clinical diagnosis. If lesions have been treated with a topical corticosteroid, they typically seem to improve as
inflammation is reduced (tinea incognito) but recur when treatments are stopped. (See "Dermatophyte (tinea) infections", section on 'Tinea faciei'.)

Other

● Flushing – Flushing is characterized by the sudden and transient appearance of facial erythema. The etiology and clinical manifestations of flushing are discussed separately [23].
(See "Approach to flushing in adults".)

● Ruddy complexion – Generalized redness of the skin may occur as a normal feature in some individuals with fair skin (eg, Fitzpatrick skin phototype I or II (table 1)). Unlike
erythematotelangiectatic rosacea, redness is not limited to the central face.

● Keratosis pilaris rubra – Keratosis pilaris rubra faciei is most common in children, adolescents, and young adults with fair complexions. Triangular erythematous patches are
present on the bilateral cheeks (picture 22). Follicular keratotic papules are located within the areas of redness, giving the skin a rough texture [24]. Clinical examination is usually
sufficient for diagnosis.

● Topical corticosteroid withdrawal – Some patients develop a red face from prolonged use of moderate to high potency topical corticosteroids on the face. Symptoms of burning or
stinging develop within several days after applications are stopped or reduced. Diagnostic difficulties arise from the inability to clearly distinguish the redness from topical
corticosteroid withdrawal from the redness due to exacerbation of the underlying dermatosis. Features suggesting topical corticosteroid withdrawal include the appearance of
generalized redness of the face within four days of withdrawal [25] and symptoms of pain, especially burning sensations [26,27].

● Burning face syndrome (facial erythrodysesthesia) – Painful or burning sensations are associated with facial erythema due to mild dilation of blood vessels. Some patients have
rosacea, while others seem to have a neuropathic pain syndrome [28].

PATIENT ASSESSMENT — The first step for narrowing the differential diagnosis of facial erythema is the performance of a thorough patient history and skin examination. The recognition
of associated symptoms, exacerbating factors, lesion time course, and subtle clinical features of the affected area are often valuable for diagnosis. In addition, the performance of a full
skin examination may yield additional skin findings that suggest an underlying cutaneous or systemic disorder.

The clinician should consider the following points during the patient evaluation:

● What are the physical characteristics of the eruption?

• Diffuse and symmetrical without scale: Ruddy complexion, flushing

• Diffuse and symmetrical with scale: Irritant contact dermatitis, airborne allergic contact dermatitis, atopic dermatitis in infants

• Symmetrical, central face or cheeks without scale: Rosacea, erythema infectiosum, keratosis pilaris rubra faciei

• Symmetrical, central face with scale: Seborrheic dermatitis, atopic dermatitis, psoriasis

• Photodistributed: Sunburn, polymorphous light eruption, phototoxic reaction, photoallergic reaction, photodamage, acute cutaneous lupus erythematosus, dermatomyositis,
lupus erythematosus tumidus

• Localized plaques or patches: Erysipelas, lupus tumidus erythematosus, cutaneous lymphoid hyperplasia, Jessner’s lymphocytic infiltrate, granuloma faciale

• Presence of telangiectasias: Photodamage, rosacea

● Are there associated symptoms?

• Prominent pruritus: Allergic contact dermatitis, atopic dermatitis, photoallergic reaction

• Painful or burning sensations: Sunburn, irritant contact dermatitis, phototoxicity, erysipelas, rosacea

● How long has the eruption been present; how long do symptoms last?

• Acute: Allergic contact dermatitis, atopic dermatitis flare, erythema infectiosum and other viral infections, sunburn, phototoxic reaction, photoallergic reaction

• Transient: Flushing

● Has the patient applied any products to the skin that could cause an irritant or allergic reaction?

• Allergic contact dermatitis, irritant contact dermatitis, photoallergic reaction

● Is the eruption exacerbated by sun exposure?

• Sunburn, phototoxic reaction, photoallergic reaction, acute cutaneous lupus erythematosus, dermatomyositis, lupus tumidus erythematosus

● Is the patient ingesting any photosensitizing medications or supplements?

• Phototoxic reaction, occasionally photoallergic reactions

● Are other body sites involved, and in what distribution?

• Psoriasis, atopic dermatitis, seborrheic dermatitis, viral exanthems, drug eruptions, photodermatoses, erythroderma, other disorders

DIAGNOSTIC TESTS — The workup of patients with facial redness is dependent upon the disorders suspected as a result of the clinical assessment. Diagnostic tests that can be useful
for the evaluation of select patients include:

● Patch testing
● Skin biopsy
● Directed serologic studies (eg, investigative tests for autoimmune disease)

Patch testing — Patch testing can be useful for identifying the causative allergen in patients with contact dermatitis. The procedure is most appropriate for patients in whom an allergic
contact dermatitis is strongly suspected (eg, history of contact with a potential allergen, paroxysmal nature of eruptions, or severe pruritus) or in patients with persistent, pruritic,
eczematous facial eruptions without another identifiable cause. (See "Patch testing".)

The results of patch testing must be interpreted carefully since a positive patch test result does not definitively indicate that a specific allergen is the cause of dermatitis. A thorough patient
interview prior to patch testing and reevaluation following the elimination of the identified allergen are essential for confirming the relevance of patch test results.

Biopsy — Skin biopsies are not necessary in most patients with facial erythema, as a thorough clinical history and skin examination often yields the diagnosis. However, in cases in which
the diagnosis remains uncertain and the disorders being considered have distinctive histopathological findings, skin biopsies can be of value.

Punch biopsies are typically performed for the evaluation of facial dermatoses as they allow for the evaluation of the full thickness of the epidermis and dermis through the removal of a
relatively small skin sample. We most commonly perform 3 mm punch biopsies when evaluating inflammatory facial dermatoses. Larger punch biopsies are typically avoided to minimize
scarring, and smaller biopsies may increase the risk for inconclusive histopathologic results. (See "Skin biopsy techniques", section on 'Punch biopsy'.)

If multiple sites are acceptable for biopsy, a site that minimizes cosmetic disfigurement should be selected.

Serology and other tests — Serologic studies and other investigative tests may be useful in the diagnostic work-up of patients with facial redness related to systemic disorders such as
acute cutaneous lupus erythematosus, dermatomyositis, or certain infections. The selection of studies is based upon the clinical suspicion for specific underlying disorders. (See
"Diagnosis and differential diagnosis of systemic lupus erythematosus in adults" and "Systemic lupus erythematosus (SLE) in children: Clinical manifestations and diagnosis", section on
'Diagnosis' and "Diagnosis and differential diagnosis of dermatomyositis and polymyositis in adults" and "Juvenile dermatomyositis and polymyositis: Diagnosis".)

TOPICAL CORTICOSTEROID USE — The treatment of facial erythema should be selected based upon the measures appropriate for the specific underlying disorder. For corticosteroid-
responsive inflammatory dermatoses, low potency agents (eg, hydrocortisone 1% or 2.5%) are most frequently employed to minimize risk for the induction of acneiform eruptions and
cutaneous atrophy that may lead to telangiectasias and a red hue to the skin (table 2).

With the exception of specific disorders in which higher potency topical corticosteroids are required (eg, discoid lupus erythematosus), the use of medium or high potency topical
corticosteroids for inflammatory facial dermatoses generally is not recommended. Facial dermatoses requiring treatment with medium or high potency topical corticosteroids are best
managed by a dermatologist. (See "General principles of dermatologic therapy and topical corticosteroid use", section on 'Side effects'.)

INDICATIONS FOR REFERRAL — Evaluation by a dermatologist is appropriate for patients with facial redness of unknown cause or that fails to respond as expected to therapy. Facial
biopsies and patch testing are best performed by clinicians trained in these procedures. (See 'Patch testing' above and 'Biopsy' above.)

SUMMARY AND RECOMMENDATIONS

● Facial redness is a common cutaneous finding that may occur as a normal feature or as a consequence of cutaneous or systemic disorders. Examples of conditions that may lead to
facial redness include inflammatory skin disease, photosensitive disorders, autoimmune disorders, vascular reactions, and infections. (See 'Etiology' above.)

● The evaluation of the patient with facial redness begins with a thorough patient history and whole body skin examination. Details such as the features of cutaneous lesions,
symptoms, duration of the eruption, and exacerbating factors should be assessed. (See 'Patient assessment' above.)

● Although the diagnosis of disorders of facial erythema can commonly be made based upon the patient history and clinical examination, patch testing, skin biopsy, or laboratory
studies may be beneficial in select patients. Obtainment of antinuclear antibody testing is not indicated in all patients with facial redness. (See 'Diagnostic tests' above.)

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REFERENCES

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Acad Dermatol 2002; 46:584.
2. Naldi L, Rebora A. Clinical practice. Seborrheic dermatitis. N Engl J Med 2009; 360:387.
3. Leung DY, Bieber T. Atopic dermatitis. Lancet 2003; 361:151.
4. Nosbaum A, Vocanson M, Rozieres A, et al. Allergic and irritant contact dermatitis. Eur J Dermatol 2009; 19:325.
5. Hönigsmann H. Polymorphous light eruption. Photodermatol Photoimmunol Photomed 2008; 24:155.
6. Millard TP, Hawk JL. Photosensitivity disorders: cause, effect and management. Am J Clin Dermatol 2002; 3:239.
7. Zuba EB, Koronowska S, Osmola-Mańkowska A, Jenerowicz D. Drug-induced Photosensitivity. Acta Dermatovenerol Croat 2016; 24:55.
8. Choi D, Kannan S, Lim HW. Evaluation of patients with photodermatoses. Dermatol Clin 2014; 32:267.
9. González E, González S. Drug photosensitivity, idiopathic photodermatoses, and sunscreens. J Am Acad Dermatol 1996; 35:871.
10. Helfrich YR, Maier LE, Cui Y, et al. Clinical, Histologic, and Molecular Analysis of Differences Between Erythematotelangiectatic Rosacea and Telangiectatic Photoaging. JAMA
Dermatol 2015; 151:825.
11. Kazandjieva J, Tsankov N, Pramatarov K. The red face revisited: connective tissue disorders. Clin Dermatol 2014; 32:153.
12. Walling HW, Sontheimer RD. Cutaneous lupus erythematosus: issues in diagnosis and treatment. Am J Clin Dermatol 2009; 10:365.
13. Costner MI, Grau RH. Update on connective tissue diseases in dermatology. Semin Cutan Med Surg 2006; 25:207.
14. Vafaie J, Schwartz RA. Erythema infectiosum. J Cutan Med Surg 2005; 9:159.
15. Bonnetblanc JM, Bédane C. Erysipelas: recognition and management. Am J Clin Dermatol 2003; 4:157.
16. Choonhakarn C, Poonsriaram A, Chaivoramukul J. Lupus erythematosus tumidus. Int J Dermatol 2004; 43:815.
17. Obermoser G, Sontheimer RD, Zelger B. Overview of common, rare and atypical manifestations of cutaneous lupus erythematosus and histopathological correlates. Lupus 2010;
19:1050.
18. Poenitz N, Dippel E, Klemke CD, et al. Jessner's lymphocytic infiltration of the skin: a CD8+ polyclonal reactive skin condition. Dermatology 2003; 207:276.
19. Rémy-Leroux V, Léonard F, Lambert D, et al. Comparison of histopathologic-clinical characteristics of Jessner's lymphocytic infiltration of the skin and lupus erythematosus tumidus:
Multicenter study of 46 cases. J Am Acad Dermatol 2008; 58:217.
20. Thiyanaratnam J, Doherty SD, Krishnan B, Hsu S. Granuloma faciale: Case report and review. Dermatol Online J 2009; 15:3.
21. Colli C, Leinweber B, Müllegger R, et al. Borrelia burgdorferi-associated lymphocytoma cutis: clinicopathologic, immunophenotypic, and molecular study of 106 cases. J Cutan
Pathol 2004; 31:232.
22. Mullegger RR. Dermatological manifestations of Lyme borreliosis. Eur J Dermatol 2004; 14:296.
23. İkizoğlu G. Red face revisited: Flushing. Clin Dermatol 2014; 32:800.
24. Marqueling AL, Gilliam AE, Prendiville J, et al. Keratosis pilaris rubra: a common but underrecognized condition. Arch Dermatol 2006; 142:1611.
25. Rapaport MJ, Rapaport V. Eyelid dermatitis to red face syndrome to cure: clinical experience in 100 cases. J Am Acad Dermatol 1999; 41:435.
26. Rapaport MJ, Lebwohl M. Corticosteroid addiction and withdrawal in the atopic: the red burning skin syndrome. Clin Dermatol 2003; 21:201.
27. Hajar T, Leshem YA, Hanifin JM, et al. A systematic review of topical corticosteroid withdrawal ("steroid addiction") in patients with atopic dermatitis and other dermatoses. J Am
Acad Dermatol 2015; 72:541.
28. Affleck A, Stewart M. Burning red face syndrome: a heterogeneous group of facial erythrodysaesthesias. Clin Exp Dermatol 2016; 41:430.

Topic 13686 Version 10.0


GRAPHICS

Rosacea

Centrofacial redness with telangiectasias in rosacea.

Reproduced with permission from: www.visualdx.com. Copyright Logical


Images, Inc.

Graphic 77020 Version 5.0


Rosacea

Erythema and telangiectasias on the cheek.

Reproduced with permission from: www.visualdx.com. Copyright Logical


Images, Inc.

Graphic 56083 Version 5.0


Perioral dermatitis

Small acne-like papules and scale are typically present in perioral


dermatitis. The skin nearest to the mouth is characteristically spared.

Reproduced with permission from: Goodheart HP. Goodheart's Photoguide of


Common Skin Disorders, 2nd ed. Lippincott Williams & Wilkins, Philadelphia
2003. Copyright ©2003 Lippincott Williams & Wilkins.

Graphic 73779 Version 2.0


Seborrheic dermatitis

Facial redness and scale involving the nasolabial folds and central face.

Reproduced with permission from: Goodheart HP. Goodheart's photoguide of


common skin disorders, 2nd ed, Lippincott Williams & Wilkins, Philadelphia
2003. Copyright © 2003 Lippincott Williams & Wilkins.

Graphic 56410 Version 4.0


Facial seborrheic dermatitis

Intense erythema and scaling involving the central face and nasolabial folds.

Graphic 59104 Version 3.0


Atopic dermatitis - infantile

Hyperpigmented, lichenified patches are present on the face of this


infant with atopic dermatitis.

Reproduced with permission from: www.visualdx.com. Copyright Logical


Images, Inc.

Graphic 77386 Version 9.0


Atopic dermatitis: Infantile

Confluent erythema, microvesiculation, scaling, and crusting on the


face, with similar involvement (to a lesser degree) on the trunk and
arms. The facial involvement is more severe due to easier access to
scratching; the baby is squeezing the breast skin to relieve the intense
pruritus.

Reproduced with permission from: Fitzpatrick TB, Johnson RA, Wolff K, et al


(Eds). Color Atlas and Synopsis of Clinical Dermatology, 3rd ed, McGraw-Hill,
New York, 1997. Copyright © McGraw-Hill.

Graphic 77457 Version 3.0


Atopic dermatitis: Infantile

Confluent erythema, microvesiculation, papules, crust, and scale on the


face of an infant.

Reproduced with permission from: Fitzpatrick TB, Johnson RA, Wolff K, et al


(Eds), Color Atlas and Synopsis of Clinical Dermatology, 3rd ed, McGraw-Hill,
New York 1997. Copyright © McGraw-Hill.

Graphic 56461 Version 4.0


Atopic dermatitis

Erythema and scale on the periocular skin in atopic dermatitis. The pruritus
associated with eyelid involvement can be severe.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 75681 Version 4.0


Atopic dermatitis

Slightly lichenified dermatitic plaques are present on the face. Erythema is


subtle in this dark-skinned patient.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 56815 Version 3.0


Dennie-Morgan fold in atopic dermatitis

An extra skin fold is present under the eyes in this patient with facial atopic
dermatitis.

Goodheart HP. Goodheart's Photoguide of Common Skin Disorders, 2nd ed, Lippincott
Williams & Wilkins, Philadelphia 2003.

Graphic 62145 Version 1.0


Psoriasis

On the face, the appearance of psoriasis is often more eczematous than


papulosquamous. Most patients with facial psoriasis also have extensive
generalized psoriasis.

Reproduced with permission from: www.visualdx.com. Copyright Logical


Images, Inc.

Graphic 79191 Version 4.0


Psoriasis

Erythematous, scaly plaques are present on the face.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 68576 Version 3.0


Allergic contact dermatitis

An intense inflammatory eruption is present on the face.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 67215 Version 3.0


Allergic contact dermatitis

Acute allergic contact dermatitis is severely pruritic. Skin often weeps.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 82705 Version 4.0


Polymorphous light eruption

This 12-year-old girl developed a pruritic eruption that consisted of


discrete and coalescing erythematous papules on the face. The lesions
were photodistributed and appeared within hours after intense sun
exposure in the spring.

Copyright © Bernard Cohen, MD, Dermatlas; http://www.dermatlas.org.

Graphic 51455 Version 6.0


Phototoxic eruption

Diffuse, sunburn-like erythema is present on the face and ears.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 69140 Version 7.0


Photoallergic eruption

This 45-year-old woman developed an acute, well-demarcated,


erythematous plaque with vesicles after topical application of ketoprofen
gel followed by sun exposure. The patient wore socks, which protected
the foot from the sun, creating the line of demarcation that is visible in
the image.

Copyright © Eric Ehrsam, MD, Dermatlas; http://www.dermatlas.org.

Graphic 63557 Version 8.0


Poikiloderma of Civatte

Chronic sun damage is associated with the development of poikiloderma


of Civatte, which typically presents as redness, telangiectasias, and
mottled hyperpigmentation on the lateral neck.

Reproduced with permission from: www.visualdx.com. Copyright Logical


Images, Inc.

Graphic 81779 Version 4.0


Acute cutaneous lupus erythematosus

Malar erythema and subtle edema are present in this patient with systemic lupus
erythematosus.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 75781 Version 4.0


Heliotrope eruption in dermatomyositis

Violaceous erythema is present on the periorbital skin in this patient


with dermatomyositis.

Reproduced with permission from: www.visualdx.com. Copyright Logical


Images, Inc.

Graphic 56879 Version 4.0


Heliotrope eruption in dermatomyositis

Violaceous erythema and edema is present on the upper eyelid in this


patient with dermatomyositis.

Reproduced with permission from: www.visualdx.com. Copyright Logical


Images, Inc.

Graphic 68649 Version 6.0


Erythema infectiosum

Redness appears acutely on one or both cheeks ("slapped cheek"


appearance). The redness may be reticulated.

Reproduced with permission from: www.visualdx.com. Copyright Logical


Images, Inc.

Graphic 52251 Version 5.0


Measles

Numerous erythematous macules are present on the face and trunk.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 61958 Version 3.0


Measles

Numerous erythematous macules are present on the face.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 73806 Version 3.0


Erysipelas

Erysipelas lesions are raised above the level of surrounding skin, and
there is a clear line of demarcation between involved and uninvolved
tissue.

Reproduced with permission from: www.visualdx.com. Copyright Logical


Images, Inc.

Graphic 67112 Version 5.0


Lupus erythematosus tumidus

Inflammatory plaques consistent with lupus erythematousus tumidus (tumid


lupus erythematosus) are present on the face.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 71792 Version 3.0


Jessner's lymphocytic infiltration of the skin

Annular erythematous plaques are present on the face.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 76268 Version 3.0


Jessner's lymphocytic infiltration of the skin

An erythematous, round plaque is present on the lateral forehead.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 62419 Version 3.0


Granuloma faciale

A red-brown plaque is present on the face.

Reproduced with permission from: www.visualdx.com. Copyright Logical


Images, Inc.

Graphic 50769 Version 3.0


Tinea faciei

An erythematous, oval plaque and pustules on the face.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 78234 Version 6.0


Fitzpatrick skin phototypes

Skin type Unexposed skin color Reaction to sun exposure*


I White Always burns, never tans

II White Always burns, minimal tan

III White to olive Burns minimally, gradually tans

IV Light brown Burns minimally, tans well

V Brown Very rarely burns, tans profusely

VI Dark brown to black Never burns, tans deeply

Note: Slight variations on the definitions of the phototypes appear in the literature.

* After the first one hour of sun exposure on untanned skin on the first day of spring.

Graphic 60541 Version 4.0


Keratosis pilaris rubra faciei

Multiple small, follicularly-based, rough, keratotic papules are present on the


cheeks. As shown here, background erythema may also be present in patients
with this condition.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 77270 Version 4.0


Comparison of representative topical corticosteroid preparations (classified according to the US system)

Available strength(s),
Trade names
Potency group* Corticosteroid Vehicle type/form percent
(United States)
(except as noted)
Super-high potency Betamethasone dipropionate, Ointment, optimized Diprolene 0.05
(group 1) augmented
Lotion Diprolene 0.05

Gel Diprolene 0.05

Clobetasol propionate Ointment Temovate 0.05

Cream Temovate 0.05

Cream, emollient base Temovate E 0.05

Gel Temovate 0.05

Lotion Clobex 0.05

Foam aerosol Olux-E 0.05

Foam aerosol (scalp) Olux 0.05

Shampoo Clobex 0.05

Solution (scalp) Temovate, Cormax 0.05

Spray aerosol Clobex 0.05

Diflucortolone valerate (not Ointment, oily cream Nerisone Forte (United 0.3
available in United States) Kingdom, others)

Fluocinonide Cream Vanos 0.1

Flurandrenolide Tape (roll) Cordran 4 mcg/cm 2

Halobetasol propionate Ointment Ultravate 0.05

Cream Ultravate 0.05

Lotion Ultravate 0.05

High potency Amcinonide Ointment Cyclocort ¶, Amcort ¶ 0.1


(group 2)
Betamethasone dipropionate Ointment Diprosone 0.05

Cream, augmented formulation Diprolene AF 0.05


(AF)

Desoximetasone Ointment Topicort 0.25

Cream Topicort 0.25

Gel Topicort 0.05

Diflorasone diacetate Ointment ApexiCon ¶, Florone ¶ 0.05

Cream, emollient ApexiCon E 0.05

Fluocinonide Ointment Lidex ¶ 0.05

Gel Lidex ¶ 0.05

Cream anhydrous Lidex ¶ 0.05

Solution Lidex ¶ 0.05

Halcinonide Ointment Halog 0.1

Cream Halog 0.1

High potency Amcinonide Cream Cyclocort ¶, Amcort ¶ 0.1


(group 3)
Lotion Amcort ¶ 0.1

Betamethasone dipropionate Cream, hydrophilic emollient Diprosone 0.05

Betamethasone valerate Ointment Valisone ¶ 0.1

Foam Luxiq 0.12

Desoximetasone Cream Topicort LP 0.05

Diflorasone diacetate Cream Florone ¶ 0.05

Diflucortolone valerate (not Cream, oily cream, ointment Nerisone (Canada, United 0.1
available in United States) Kingdom, others)

Fluocinonide Cream aqueous emollient Lidex-E ¶ 0.05

Fluticasone propionate Ointment Cutivate 0.005

Mometasone furoate Ointment Elocon 0.1

Triamcinolone acetonide Ointment Kenalog ¶ 0.5

Cream Triderm, Aristocort HP ¶ 0.5

Medium potency Betamethasone dipropionate Spray Sernivo 0.05


(group 4)
Clocortolone pivalate Cream Cloderm 0.1

Fluocinolone acetonide Ointment Synalar ¶ 0.025

Flurandrenolide Ointment Cordran 0.05

Hydrocortisone valerate Ointment Westcort 0.2

Mometasone furoate Cream Elocon 0.1

Lotion Elocon 0.1

Solution Elocon ¶ 0.1

Triamcinolone acetonide Cream Kenalog ¶ 0.1

Ointment Kenalog ¶ 0.1

Aerosol spray Kenalog 0.2 mg per 2 second spray

Lower-mid potency Betamethasone dipropionate Lotion Diprosone 0.05


(group 5)
Betamethasone valerate Cream Beta-Val, Valisone ¶ 0.1

Desonide Ointment DesOwen, Tridesilon ¶ 0.05

Gel Desonate 0.05

Fluocinolone acetonide Cream Synalar ¶ 0.025

Flurandrenolide Cream Cordran 0.05

Lotion Cordran 0.05

Fluticasone propionate Cream Cutivate 0.05

Lotion Cutivate 0.05

Hydrocortisone butyrate Ointment Locoid 0.1

Cream Locoid, Locoid Lipocream 0.1

Lotion, spray Cortizone 10 maximum 0.1

Lotion Locoid 0.1

Solution Locoid 0.1

Hydrocortisone probutate Cream Pandel 0.1

Hydrocortisone valerate Cream Westcort ¶ 0.2

Prednicarbate Cream, emollient Dermatop 0.1

Ointment Dermatop 0.1

Triamcinolone acetonide Lotion Kenalog ¶ 0.1

Ointment Kenalog ¶ 0.025

Low potency Alclometasone dipropionate Ointment Aclovate 0.05


(group 6)
Cream Aclovate 0.05

Betamethasone valerate Lotion Beta-Val, Valisone ¶ 0.1

Desonide Cream DesOwen, Tridesilon ¶ 0.05

Lotion DesOwen, LoKara 0.05

Foam Verdeso 0.05

Fluocinolone acetonide Cream Synalar ¶ 0.01

Solution Synalar ¶ 0.01

Shampoo Capex 0.01

Oil (scalp) Δ Derma-Smoothe/FS Scalp 0.01

Oil (body) Δ Derma-Smoothe/FS Body 0.01

Triamcinolone acetonide Cream Kenalog ¶, Aristocort ¶ 0.025

Lotion Kenalog ¶ 0.025

Least potent Hydrocortisone (base, ≥2%) Ointment Hytone 2.5


(group 7)
Cream Hytone, Nutracort ¶ 2.5

Lotion Hytone, Ala Scalp, Scalacort 2.5 or 2

Solution Texacort 2.5

Hydrocortisone (base, <2%) Ointment Cortaid, Hytone, Nutracort 1

Cream Cortaid, Hytone, Synacort 1

Lotion Aquanil HC, Sarnol-HC, 1


Cortizone 10

Spray Cortaid 1

Solution Cortaid, Noble, Scalp relief 1

Ointment Cortaid 0.5

Cream Cortaid 0.5

Hydrocortisone acetate with Ointment Pramosone 1 or 2.5


pramoxine 1% combination
Cream Pramosone, Analpram-HC 1 or 2.5

Lotion Pramosone, Analpram-HC 1 or 2.5

Aerosol foam Epifoam 1

US: United States.


* Listed by potency according to the US classification system: group 1 is the most potent, group 7 is the least potent. Other countries use a different classification system with
only four or five groups.
¶ Inactive United States trade name for specific product; brand may be available outside United States.
Δ 48% refined peanut oil.

Data from:
1. Lexicomp Online. Copyright © 1978-2017 Lexicomp, Inc. All Rights Reserved.
2. Tadicherla S, Ross K, Shenefelt D. Topical corticosteroids in dermatology. Journal of Drugs in Dermatology 2009; 12:1093.
3. U.S. Food & Drug Administration Approved Drug Products with Therapeutic Equivalence (Orange Book). Available at:
https://www.accessdata.fda.gov/scripts/cder/ob/default.cfm (Accessed on June 18, 2017).

Graphic 62402 Version 42.0

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