Richard P. Usatine, MD

An 8-year-old girl was brought to her family physician’s office (RU) because of a persistent rash on her lateral eyebrows and periumbilical region. The family indicated that she’d had the rash for more than 6 months. They also mentioned that the child had received a new pair of eyeglasses 8 months earlier. The child was otherwise in good health. The physical examination revealed erythematous scaling plaques near both lateral eyebrows and around the belly button (FIGURES 1 AND 2).

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

We recognized that this was a case of allergic contact dermatitis (ACD), based on the clinical presentation. The distribution of the erythema, scale, and postinflammatory hyperpigmentation was highly suggestive of an ACD to nickel. In this case, the nickel in the patient’s eyeglasses and the snaps found on her pants were the culprits.

The lichenification of the plaque near the umbilicus suggested that the dermatitis was not acute and that the patient had likely been scratching the area due to itching. The plaque near the patient’s eye was actually in the shape of the metal on the inside of her glasses.

Most prevalent contact allergens. Patch testing data indicate that the 5 most prevalent contact allergens out of more than 3700 that are known are: nickel (14.3% of patients tested), fragrance mix (14%), the topical antibiotic neomycin (11.6%), balsam of Peru (used in some perfumes, toiletries, and pharmaceutical items) (10.4%), and the mercury-based vaccine preservative thimerosal (10.4%).¹

The 5 most prevalent contact allergens are nickel, fragrance mix, neomycin, balsam of Peru, and thimerosal.

ACD is a delayed-type hypersensitivity reaction in which a foreign substance comes into contact with the skin and is linked to skin proteins forming an antigen complex that leads to sensitization. When the epidermis is re-exposed to the antigen, the sensitized T cells initiate an inflammatory cascade, leading to the skin changes seen in ACD.²

Silverberg et al reported that in 30 children with a personal history of umbilical or wrist dermatitis or a family history of nickel ACD, 100% demonstrated a positive reaction to nickel sulfate.³ Nickel continues to be used (and unregulated) in a wide range of products, including costume jewelry, piercing posts, belt buckles, eyeglasses, and personal electronics (eg, tablets, cell phones, and laptop computers).

Making the diagnosis. Contact dermatitis can sometimes be diagnosed clinically with a good history and physical exam. However, there are many cases in which patch testing is needed to find the offending allergens or confirm the suspicion regarding a specific allergen. The only convenient and ready-to-use patch test in the United States is the T.R.U.E. test.

The differential includes other superficial skin infections

ACD characteristically presents with eczematoid plaques that are primarily in the area(s) of cutaneous contact with an allergen. The condition typically appears within a few days of exposure.

The differential diagnosis for ACD includes cutaneous candidiasis, impetigo, plaque psoriasis, and seborrheic dermatitis.

Cutaneous candidiasis is a superficial infection of the skin with a candida species. It can present as beefy red erythematous plaques on the buttocks, lower abdomen, thighs, or in intertriginous areas or oral commissures. A hallmark sign is pinpoint pustulovesicular satellite lesions.

Impetigo is a superficial bacterial skin infection that presents with edema, erythema, tenderness on palpation, and possible purulent drainage. It appears as honey-colored crusts with erythema and occurs most often on the face—especially around a child’s nose and mouth—but can occur anywhere on the head and body.

Plaque psoriasis presents as erythematous silver-scaled plaques on extensor surfaces, including the elbows and knees. Inverse psoriasis may present as erythema and maceration in intertriginous areas.

Seborrheic dermatitis appears as well-circumscribed greasy scale overlying erythematous skin. It is commonly found on the scalp, eyebrows, nasolabial folds, chest, face, and in the ear canals. It is thought to be an inflammatory reaction to Malassezia furfur.

Cool compresses, topical steroids can relieve symptoms

Patients with ACD should avoid the allergen that is causing the reaction. In cases of nickel ACD, the patient may cover the metal tab of their jeans with an iron-on patch or a few coats of clear nail polish. A better option is to buy jeans and pants that do not have nickel in the metal tab. (Levi’s has removed nickel from their pants.) Cool compresses can soothe the symptoms of acute cases of ACD.⁴ Calamine and colloidal oatmeal baths may help to dry and soothe acute, oozing lesions. Localized acute ACD lesions respond best to mid-potency (eg, 0.1% triamcinolone) to high-potency (eg, 0.05% clobetasol) topical steroids.⁴

On areas of thinner skin (eg, flexural surfaces, eyelids, face, anogenital region), lower-potency steroids such as desonide ointment can minimize the risk of skin atrophy.^3,4 Be aware that some patients are actually allergic to topical steroids. This unfortunate situation can be diagnosed with patch testing.

We recommended that our patient get different glasses that were nickel-free. Fortunately, there are many frames for glasses that have no nickel in them. We also gave her advice on how to avoid the nickel that still exists in some pants. We gave her desonide 0.05% cream to apply to the affected area for symptomatic relief.

CORRESPONDENCE
Richard P. Usatine, MD, Skin clinic, University of Texas Health Science Center at San Antonio, 903 W. Martin, San Antonio, TX 78207; [email protected].

An 8-year-old girl was brought to her family physician’s office (RU) because of a persistent rash on her lateral eyebrows and periumbilical region. The family indicated that she’d had the rash for more than 6 months. They also mentioned that the child had received a new pair of eyeglasses 8 months earlier. The child was otherwise in good health. The physical examination revealed erythematous scaling plaques near both lateral eyebrows and around the belly button (FIGURES 1 AND 2).

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

We recognized that this was a case of allergic contact dermatitis (ACD), based on the clinical presentation. The distribution of the erythema, scale, and postinflammatory hyperpigmentation was highly suggestive of an ACD to nickel. In this case, the nickel in the patient’s eyeglasses and the snaps found on her pants were the culprits.

The lichenification of the plaque near the umbilicus suggested that the dermatitis was not acute and that the patient had likely been scratching the area due to itching. The plaque near the patient’s eye was actually in the shape of the metal on the inside of her glasses.

Most prevalent contact allergens. Patch testing data indicate that the 5 most prevalent contact allergens out of more than 3700 that are known are: nickel (14.3% of patients tested), fragrance mix (14%), the topical antibiotic neomycin (11.6%), balsam of Peru (used in some perfumes, toiletries, and pharmaceutical items) (10.4%), and the mercury-based vaccine preservative thimerosal (10.4%).¹

The 5 most prevalent contact allergens are nickel, fragrance mix, neomycin, balsam of Peru, and thimerosal.

ACD is a delayed-type hypersensitivity reaction in which a foreign substance comes into contact with the skin and is linked to skin proteins forming an antigen complex that leads to sensitization. When the epidermis is re-exposed to the antigen, the sensitized T cells initiate an inflammatory cascade, leading to the skin changes seen in ACD.²

Silverberg et al reported that in 30 children with a personal history of umbilical or wrist dermatitis or a family history of nickel ACD, 100% demonstrated a positive reaction to nickel sulfate.³ Nickel continues to be used (and unregulated) in a wide range of products, including costume jewelry, piercing posts, belt buckles, eyeglasses, and personal electronics (eg, tablets, cell phones, and laptop computers).

Making the diagnosis. Contact dermatitis can sometimes be diagnosed clinically with a good history and physical exam. However, there are many cases in which patch testing is needed to find the offending allergens or confirm the suspicion regarding a specific allergen. The only convenient and ready-to-use patch test in the United States is the T.R.U.E. test.

The differential includes other superficial skin infections

ACD characteristically presents with eczematoid plaques that are primarily in the area(s) of cutaneous contact with an allergen. The condition typically appears within a few days of exposure.

The differential diagnosis for ACD includes cutaneous candidiasis, impetigo, plaque psoriasis, and seborrheic dermatitis.

Cutaneous candidiasis is a superficial infection of the skin with a candida species. It can present as beefy red erythematous plaques on the buttocks, lower abdomen, thighs, or in intertriginous areas or oral commissures. A hallmark sign is pinpoint pustulovesicular satellite lesions.

Impetigo is a superficial bacterial skin infection that presents with edema, erythema, tenderness on palpation, and possible purulent drainage. It appears as honey-colored crusts with erythema and occurs most often on the face—especially around a child’s nose and mouth—but can occur anywhere on the head and body.

Plaque psoriasis presents as erythematous silver-scaled plaques on extensor surfaces, including the elbows and knees. Inverse psoriasis may present as erythema and maceration in intertriginous areas.

Seborrheic dermatitis appears as well-circumscribed greasy scale overlying erythematous skin. It is commonly found on the scalp, eyebrows, nasolabial folds, chest, face, and in the ear canals. It is thought to be an inflammatory reaction to Malassezia furfur.

Cool compresses, topical steroids can relieve symptoms

Patients with ACD should avoid the allergen that is causing the reaction. In cases of nickel ACD, the patient may cover the metal tab of their jeans with an iron-on patch or a few coats of clear nail polish. A better option is to buy jeans and pants that do not have nickel in the metal tab. (Levi’s has removed nickel from their pants.) Cool compresses can soothe the symptoms of acute cases of ACD.⁴ Calamine and colloidal oatmeal baths may help to dry and soothe acute, oozing lesions. Localized acute ACD lesions respond best to mid-potency (eg, 0.1% triamcinolone) to high-potency (eg, 0.05% clobetasol) topical steroids.⁴

On areas of thinner skin (eg, flexural surfaces, eyelids, face, anogenital region), lower-potency steroids such as desonide ointment can minimize the risk of skin atrophy.^3,4 Be aware that some patients are actually allergic to topical steroids. This unfortunate situation can be diagnosed with patch testing.

We recommended that our patient get different glasses that were nickel-free. Fortunately, there are many frames for glasses that have no nickel in them. We also gave her advice on how to avoid the nickel that still exists in some pants. We gave her desonide 0.05% cream to apply to the affected area for symptomatic relief.

CORRESPONDENCE
Richard P. Usatine, MD, Skin clinic, University of Texas Health Science Center at San Antonio, 903 W. Martin, San Antonio, TX 78207; [email protected].

An 8-year-old girl was brought to her family physician’s office (RU) because of a persistent rash on her lateral eyebrows and periumbilical region. The family indicated that she’d had the rash for more than 6 months. They also mentioned that the child had received a new pair of eyeglasses 8 months earlier. The child was otherwise in good health. The physical examination revealed erythematous scaling plaques near both lateral eyebrows and around the belly button (FIGURES 1 AND 2).

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

We recognized that this was a case of allergic contact dermatitis (ACD), based on the clinical presentation. The distribution of the erythema, scale, and postinflammatory hyperpigmentation was highly suggestive of an ACD to nickel. In this case, the nickel in the patient’s eyeglasses and the snaps found on her pants were the culprits.

The lichenification of the plaque near the umbilicus suggested that the dermatitis was not acute and that the patient had likely been scratching the area due to itching. The plaque near the patient’s eye was actually in the shape of the metal on the inside of her glasses.

Most prevalent contact allergens. Patch testing data indicate that the 5 most prevalent contact allergens out of more than 3700 that are known are: nickel (14.3% of patients tested), fragrance mix (14%), the topical antibiotic neomycin (11.6%), balsam of Peru (used in some perfumes, toiletries, and pharmaceutical items) (10.4%), and the mercury-based vaccine preservative thimerosal (10.4%).¹

The 5 most prevalent contact allergens are nickel, fragrance mix, neomycin, balsam of Peru, and thimerosal.

ACD is a delayed-type hypersensitivity reaction in which a foreign substance comes into contact with the skin and is linked to skin proteins forming an antigen complex that leads to sensitization. When the epidermis is re-exposed to the antigen, the sensitized T cells initiate an inflammatory cascade, leading to the skin changes seen in ACD.²

Silverberg et al reported that in 30 children with a personal history of umbilical or wrist dermatitis or a family history of nickel ACD, 100% demonstrated a positive reaction to nickel sulfate.³ Nickel continues to be used (and unregulated) in a wide range of products, including costume jewelry, piercing posts, belt buckles, eyeglasses, and personal electronics (eg, tablets, cell phones, and laptop computers).

Making the diagnosis. Contact dermatitis can sometimes be diagnosed clinically with a good history and physical exam. However, there are many cases in which patch testing is needed to find the offending allergens or confirm the suspicion regarding a specific allergen. The only convenient and ready-to-use patch test in the United States is the T.R.U.E. test.

The differential includes other superficial skin infections

ACD characteristically presents with eczematoid plaques that are primarily in the area(s) of cutaneous contact with an allergen. The condition typically appears within a few days of exposure.

The differential diagnosis for ACD includes cutaneous candidiasis, impetigo, plaque psoriasis, and seborrheic dermatitis.

Cutaneous candidiasis is a superficial infection of the skin with a candida species. It can present as beefy red erythematous plaques on the buttocks, lower abdomen, thighs, or in intertriginous areas or oral commissures. A hallmark sign is pinpoint pustulovesicular satellite lesions.

Impetigo is a superficial bacterial skin infection that presents with edema, erythema, tenderness on palpation, and possible purulent drainage. It appears as honey-colored crusts with erythema and occurs most often on the face—especially around a child’s nose and mouth—but can occur anywhere on the head and body.

Plaque psoriasis presents as erythematous silver-scaled plaques on extensor surfaces, including the elbows and knees. Inverse psoriasis may present as erythema and maceration in intertriginous areas.

Seborrheic dermatitis appears as well-circumscribed greasy scale overlying erythematous skin. It is commonly found on the scalp, eyebrows, nasolabial folds, chest, face, and in the ear canals. It is thought to be an inflammatory reaction to Malassezia furfur.

Cool compresses, topical steroids can relieve symptoms

Patients with ACD should avoid the allergen that is causing the reaction. In cases of nickel ACD, the patient may cover the metal tab of their jeans with an iron-on patch or a few coats of clear nail polish. A better option is to buy jeans and pants that do not have nickel in the metal tab. (Levi’s has removed nickel from their pants.) Cool compresses can soothe the symptoms of acute cases of ACD.⁴ Calamine and colloidal oatmeal baths may help to dry and soothe acute, oozing lesions. Localized acute ACD lesions respond best to mid-potency (eg, 0.1% triamcinolone) to high-potency (eg, 0.05% clobetasol) topical steroids.⁴

On areas of thinner skin (eg, flexural surfaces, eyelids, face, anogenital region), lower-potency steroids such as desonide ointment can minimize the risk of skin atrophy.^3,4 Be aware that some patients are actually allergic to topical steroids. This unfortunate situation can be diagnosed with patch testing.

We recommended that our patient get different glasses that were nickel-free. Fortunately, there are many frames for glasses that have no nickel in them. We also gave her advice on how to avoid the nickel that still exists in some pants. We gave her desonide 0.05% cream to apply to the affected area for symptomatic relief.

CORRESPONDENCE
Richard P. Usatine, MD, Skin clinic, University of Texas Health Science Center at San Antonio, 903 W. Martin, San Antonio, TX 78207; [email protected].

A 48-year-old woman experiencing homelessness presented to our clinic with a 4-week history of an intensely pruritic rash on her upper back and bilateral upper extremities. She reported that she had experienced exacerbations and remissions of the rash in similar locations for the past several years and during childhood. Factors that exacerbated the rash included being outdoors and being exposed to heat. Her pruritus was intensified by scratching the skin and was significantly worse at night. Previous doctors had diagnosed her with psoriasis and prescribed a short trial of hydrocortisone cream and oral antihistamines, but they provided minimal relief.

The patient indicated that the itching interrupted her sleep and her skin’s appearance made it difficult to get a job. The physical exam revealed excoriated and erythematous papules and patches on her upper back, the extensor and flexor aspects of her bilateral forearms, and the dorsal surface of her bilateral wrists, hands, and fingers (FIGURE 1). Her skin was dry and scaly with pigmentary changes and skin thickening (FIGURE 2). She denied any other systemic symptoms. Her hair and nails were normal, she had no palpable lymph nodes, and she was afebrile. She reported suffering from seasonal allergies, but wasn’t aware of a family history of skin disorders.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Chronic atopic dermatitis

Although the patient was told she had psoriasis by previous doctors, we diagnosed her condition as atopic dermatitis based on its clinical appearance. There is no single test that can establish a diagnosis of atopic dermatitis. While serum total IgE levels are often elevated, testing is not currently recommended.

The United Kingdom working group on atopic dermatitis published diagnostic criteria based on clinical history and physical exam that include pruritic skin in addition to the presence of 3 or more of the following: skin crease involvement, chronically dry skin, symptom onset before 2 years of age, and visible evidence of dermatitis involving flexural surfaces.¹ Our patient fulfilled all but one condition, as she wasn’t sure if her symptoms began before age 2.

Approximately 70% of patients with atopic dermatitis have a positive family history of an atopic disease, such as eczema, asthma, or allergic rhinitis.

Atopic dermatitis is a chronic and inflammatory cutaneous disease that affects approximately 10% to 12% of children and less than 1% of adults in the United States.² Approximately 90% of cases present before the age of 5 and the literature demonstrates a slight female predominance.^3,4

Disease severity is classified as mild, moderate, or severe.⁵ Mild disease is characterized by dry skin and minimal itching with little impairment of the patient’s physical and psychological wellbeing. Moderate disease includes frequent pruritus and erythema with or without secondary skin changes and a moderate impact on physical and mental health. In severe disease, extensive secondary skin changes exist and the patient’s daily activities, sleep, and mental health may be severely impaired.

Etiology is multifactorial. Causes of atopic dermatitis include abnormalities in the epidermal stratum corneum and tight junctions, a heightened type-2 helper T-cell response to environmental antigens, innate immunity defects, and altered microbial skin flora.^6,7

Genetic influences appear to play a substantial role in disease development. Approximately 70% of patients have a positive family history of an atopic disease such as eczema, asthma, or allergic rhinitis.⁸ Genetic defects are believed to be related to defective proteins and lipids in the epidermis that lead to disruption of the epidermal barrier and subsequent cutaneous inflammation.^6,7

Clinical presentation: Lesion distribution varies with age

Intense pruritus and dry scaly skin occur in both children and adults, although the distribution of lesions may vary with age. Children typically exhibit erythematous patches with papules and crusting on the face, scalp, extremities, or trunk. In adults, lesions are primarily located on the hands and feet, but may also present on the face, wrists, forearms, and flexural areas.³

Adults also frequently present with secondary skin changes such as thickened skin, pigmentation changes, lichenification, and excoriated papulesdue to chronic rubbing or scratching.³ Our patient presented with significant lichenification and hyperpigmentation of the skin that was most prominent on the wrists and forearms.

Additional clinical features consistent with atopic dermatitis include a personal history of allergic conditions and a disease course characterized by exacerbations and remissions. Exacerbations may be caused by heat exposure, dry climates, anxiety, rapid temperature variations, contact with certain chemical substances, or microbial infections.⁸

Differential Dx includes psoriasis and scabies

The differential diagnosis of chronic atopic dermatitis consists of allergic or irritant contact dermatitis, plaque psoriasis, seborrheic dermatitis, scabies, and drug eruptions. Early diagnosis of atopic dermatitis is imperative to prevent sleep disturbances, chronic secondary skin changes, scarring, and the development of skin infections.

Allergic or irritant contact dermatitis is a cutaneous inflammation occurring after contact with an allergen or irritant. The lesions include erythematous, scaling areas with marked borders that are commonly pruritic. Acute cases often present with vesicles and bullae, while lichenification with cracks and fissures are common among chronic cases. Patch testing may be performed if the diagnosis is suspected.

Plaque psoriasis is characterized by areas of dry, erythematous, and well-demarcated plaques with silver scales that are most commonly found on the knees, elbows, scalp, and lower back. Systemic manifestations can include joint pain and joint swelling. Nail pitting and onycholysis are also common. While our patient had skin thickening, it was from the lichenification that is common in atopic dermatitis.

Psoriasis and atopic dermatitis are often confused. Psoriasis has discrete plaques on extensor surfaces and is often associated with nail changes, while the thickening of the skin that comes with chronic itch and scratching of atopic dermatitis is often less well circumscribed and found on flexor surfaces. Family physicians are frequently the first to encounter patients with atopic dermatitis and psoriasis and must be able to distinguish these conditions, as their treatments differ.

Seborrheic dermatitis is a chronic, relapsing inflammatory condition characterized by pruritic, erythematous, greasy, scaly patches on sebum-rich skin such as the scalp, face, and upper trunk. Seborrheic dermatitis is a clinical diagnosis.

Scabies is a pruritic skin condition caused by Sarcoptes scabiei var hominis. Characteristic linear burrows often appear as serpiginous, gray, threadlike elevations in the webbed spaces of the fingers, scrotum, areolae, elbows, axillae, feet, and wrist flexors. Secondary lesions from scratching or inflammation include excoriations, erythema, and hyperpigmentation. The diagnosis is made clinically and confirmed by dermoscopy, when available. Alternatively, mites or eggs may be observed on skin scrapings using light microscopy.

Drug eruptions should be considered in individuals taking medications who develop acute, symmetric cutaneous eruptions that may be morbilliform, urticarial, papulosquamous, pustular, or bullous in nature.

Treatment depends on severity, area of involvement, and patient’s age

Components of atopic dermatitis treatment include skin hydration, negative stimuli avoidance, pharmacologic modalities, and patient education. Improved skin hydration can be achieved by applying thick emollients containing little to no water at least twice daily and after bathing.

Topical corticosteroids are added when emollient use alone fails. Potency selection is based upon the patient’s age, involved body region, and the severity of skin inflammation.⁸ In order to reduce cutaneous atrophy, only low-potency corticosteroids should be applied to the face, groin, and axillae. Patients with mild disease may apply desonide 0.05% or hydrocortisone 2.5% cream or ointment once or twice daily for 2 to 4 weeks.⁸ Patients without improvement or with moderate disease may need medium- to high-potency steroids such as fluocinolone 0.025% or triamcinolone 0.1%.

Exacerbations of atopic dermatitis may be caused by heat exposure, anxiety, rapid temperature variations, contact with certain chemical substances, or microbial infections.

Patients with atopic dermatitis on the face, eyelids, neck, and skin folds or those who do not obtain relief from combined emollients and topical corticosteroids may benefit from topical calcineurin inhibitors such as pimecrolimus or tacrolimus.⁹ However, these agents should be utilized only for short periods of time and avoided in immunocompromised patients and those younger than 2 years of age.⁹

Patients with uncontrolled moderate to severe refractory disease may consider a trial of phototherapy or cyclosporine if phototherapy is ineffective or unavailable.¹⁰ A meta-analysis has shown that once remission is achieved, intermittent therapy with moderate- to high-potency corticosteroids or tacrolimus may be effective in reducing subsequent flares.¹¹

In all cases, sedating antihistamines such as diphenhydramine or hydroxyzine can be utilized for pruritic relief, particularly at night. Additionally, signs suggestive of infection should prompt antibiotic treatment with agents that provide coverage for Staphylococcus and Streptococcus species. Lastly, patients must be adequately educated on stimuli avoidance (eg, hot water, wool) and counseled on the medical and psychological issues that often accompany atopic dermatitis.

Our patient was placed on triamcinolone 0.1% for 4 weeks and her condition improved.

CORRESPONDENCE
Andrea Richardson, MD, MPH, 7414 Carriage Bay, San Antonio, TX 78249; [email protected].

A 48-year-old woman experiencing homelessness presented to our clinic with a 4-week history of an intensely pruritic rash on her upper back and bilateral upper extremities. She reported that she had experienced exacerbations and remissions of the rash in similar locations for the past several years and during childhood. Factors that exacerbated the rash included being outdoors and being exposed to heat. Her pruritus was intensified by scratching the skin and was significantly worse at night. Previous doctors had diagnosed her with psoriasis and prescribed a short trial of hydrocortisone cream and oral antihistamines, but they provided minimal relief.

The patient indicated that the itching interrupted her sleep and her skin’s appearance made it difficult to get a job. The physical exam revealed excoriated and erythematous papules and patches on her upper back, the extensor and flexor aspects of her bilateral forearms, and the dorsal surface of her bilateral wrists, hands, and fingers (FIGURE 1). Her skin was dry and scaly with pigmentary changes and skin thickening (FIGURE 2). She denied any other systemic symptoms. Her hair and nails were normal, she had no palpable lymph nodes, and she was afebrile. She reported suffering from seasonal allergies, but wasn’t aware of a family history of skin disorders.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Chronic atopic dermatitis

Although the patient was told she had psoriasis by previous doctors, we diagnosed her condition as atopic dermatitis based on its clinical appearance. There is no single test that can establish a diagnosis of atopic dermatitis. While serum total IgE levels are often elevated, testing is not currently recommended.

The United Kingdom working group on atopic dermatitis published diagnostic criteria based on clinical history and physical exam that include pruritic skin in addition to the presence of 3 or more of the following: skin crease involvement, chronically dry skin, symptom onset before 2 years of age, and visible evidence of dermatitis involving flexural surfaces.¹ Our patient fulfilled all but one condition, as she wasn’t sure if her symptoms began before age 2.

Approximately 70% of patients with atopic dermatitis have a positive family history of an atopic disease, such as eczema, asthma, or allergic rhinitis.

Atopic dermatitis is a chronic and inflammatory cutaneous disease that affects approximately 10% to 12% of children and less than 1% of adults in the United States.² Approximately 90% of cases present before the age of 5 and the literature demonstrates a slight female predominance.^3,4

Disease severity is classified as mild, moderate, or severe.⁵ Mild disease is characterized by dry skin and minimal itching with little impairment of the patient’s physical and psychological wellbeing. Moderate disease includes frequent pruritus and erythema with or without secondary skin changes and a moderate impact on physical and mental health. In severe disease, extensive secondary skin changes exist and the patient’s daily activities, sleep, and mental health may be severely impaired.

Etiology is multifactorial. Causes of atopic dermatitis include abnormalities in the epidermal stratum corneum and tight junctions, a heightened type-2 helper T-cell response to environmental antigens, innate immunity defects, and altered microbial skin flora.^6,7

Genetic influences appear to play a substantial role in disease development. Approximately 70% of patients have a positive family history of an atopic disease such as eczema, asthma, or allergic rhinitis.⁸ Genetic defects are believed to be related to defective proteins and lipids in the epidermis that lead to disruption of the epidermal barrier and subsequent cutaneous inflammation.^6,7

Clinical presentation: Lesion distribution varies with age

Intense pruritus and dry scaly skin occur in both children and adults, although the distribution of lesions may vary with age. Children typically exhibit erythematous patches with papules and crusting on the face, scalp, extremities, or trunk. In adults, lesions are primarily located on the hands and feet, but may also present on the face, wrists, forearms, and flexural areas.³

Adults also frequently present with secondary skin changes such as thickened skin, pigmentation changes, lichenification, and excoriated papulesdue to chronic rubbing or scratching.³ Our patient presented with significant lichenification and hyperpigmentation of the skin that was most prominent on the wrists and forearms.

Additional clinical features consistent with atopic dermatitis include a personal history of allergic conditions and a disease course characterized by exacerbations and remissions. Exacerbations may be caused by heat exposure, dry climates, anxiety, rapid temperature variations, contact with certain chemical substances, or microbial infections.⁸

Differential Dx includes psoriasis and scabies

The differential diagnosis of chronic atopic dermatitis consists of allergic or irritant contact dermatitis, plaque psoriasis, seborrheic dermatitis, scabies, and drug eruptions. Early diagnosis of atopic dermatitis is imperative to prevent sleep disturbances, chronic secondary skin changes, scarring, and the development of skin infections.

Allergic or irritant contact dermatitis is a cutaneous inflammation occurring after contact with an allergen or irritant. The lesions include erythematous, scaling areas with marked borders that are commonly pruritic. Acute cases often present with vesicles and bullae, while lichenification with cracks and fissures are common among chronic cases. Patch testing may be performed if the diagnosis is suspected.

Plaque psoriasis is characterized by areas of dry, erythematous, and well-demarcated plaques with silver scales that are most commonly found on the knees, elbows, scalp, and lower back. Systemic manifestations can include joint pain and joint swelling. Nail pitting and onycholysis are also common. While our patient had skin thickening, it was from the lichenification that is common in atopic dermatitis.

Psoriasis and atopic dermatitis are often confused. Psoriasis has discrete plaques on extensor surfaces and is often associated with nail changes, while the thickening of the skin that comes with chronic itch and scratching of atopic dermatitis is often less well circumscribed and found on flexor surfaces. Family physicians are frequently the first to encounter patients with atopic dermatitis and psoriasis and must be able to distinguish these conditions, as their treatments differ.

Seborrheic dermatitis is a chronic, relapsing inflammatory condition characterized by pruritic, erythematous, greasy, scaly patches on sebum-rich skin such as the scalp, face, and upper trunk. Seborrheic dermatitis is a clinical diagnosis.

Scabies is a pruritic skin condition caused by Sarcoptes scabiei var hominis. Characteristic linear burrows often appear as serpiginous, gray, threadlike elevations in the webbed spaces of the fingers, scrotum, areolae, elbows, axillae, feet, and wrist flexors. Secondary lesions from scratching or inflammation include excoriations, erythema, and hyperpigmentation. The diagnosis is made clinically and confirmed by dermoscopy, when available. Alternatively, mites or eggs may be observed on skin scrapings using light microscopy.

Drug eruptions should be considered in individuals taking medications who develop acute, symmetric cutaneous eruptions that may be morbilliform, urticarial, papulosquamous, pustular, or bullous in nature.

Treatment depends on severity, area of involvement, and patient’s age

Components of atopic dermatitis treatment include skin hydration, negative stimuli avoidance, pharmacologic modalities, and patient education. Improved skin hydration can be achieved by applying thick emollients containing little to no water at least twice daily and after bathing.

Topical corticosteroids are added when emollient use alone fails. Potency selection is based upon the patient’s age, involved body region, and the severity of skin inflammation.⁸ In order to reduce cutaneous atrophy, only low-potency corticosteroids should be applied to the face, groin, and axillae. Patients with mild disease may apply desonide 0.05% or hydrocortisone 2.5% cream or ointment once or twice daily for 2 to 4 weeks.⁸ Patients without improvement or with moderate disease may need medium- to high-potency steroids such as fluocinolone 0.025% or triamcinolone 0.1%.

Exacerbations of atopic dermatitis may be caused by heat exposure, anxiety, rapid temperature variations, contact with certain chemical substances, or microbial infections.

Patients with atopic dermatitis on the face, eyelids, neck, and skin folds or those who do not obtain relief from combined emollients and topical corticosteroids may benefit from topical calcineurin inhibitors such as pimecrolimus or tacrolimus.⁹ However, these agents should be utilized only for short periods of time and avoided in immunocompromised patients and those younger than 2 years of age.⁹

Patients with uncontrolled moderate to severe refractory disease may consider a trial of phototherapy or cyclosporine if phototherapy is ineffective or unavailable.¹⁰ A meta-analysis has shown that once remission is achieved, intermittent therapy with moderate- to high-potency corticosteroids or tacrolimus may be effective in reducing subsequent flares.¹¹

In all cases, sedating antihistamines such as diphenhydramine or hydroxyzine can be utilized for pruritic relief, particularly at night. Additionally, signs suggestive of infection should prompt antibiotic treatment with agents that provide coverage for Staphylococcus and Streptococcus species. Lastly, patients must be adequately educated on stimuli avoidance (eg, hot water, wool) and counseled on the medical and psychological issues that often accompany atopic dermatitis.

Our patient was placed on triamcinolone 0.1% for 4 weeks and her condition improved.

CORRESPONDENCE
Andrea Richardson, MD, MPH, 7414 Carriage Bay, San Antonio, TX 78249; [email protected].

A 48-year-old woman experiencing homelessness presented to our clinic with a 4-week history of an intensely pruritic rash on her upper back and bilateral upper extremities. She reported that she had experienced exacerbations and remissions of the rash in similar locations for the past several years and during childhood. Factors that exacerbated the rash included being outdoors and being exposed to heat. Her pruritus was intensified by scratching the skin and was significantly worse at night. Previous doctors had diagnosed her with psoriasis and prescribed a short trial of hydrocortisone cream and oral antihistamines, but they provided minimal relief.

The patient indicated that the itching interrupted her sleep and her skin’s appearance made it difficult to get a job. The physical exam revealed excoriated and erythematous papules and patches on her upper back, the extensor and flexor aspects of her bilateral forearms, and the dorsal surface of her bilateral wrists, hands, and fingers (FIGURE 1). Her skin was dry and scaly with pigmentary changes and skin thickening (FIGURE 2). She denied any other systemic symptoms. Her hair and nails were normal, she had no palpable lymph nodes, and she was afebrile. She reported suffering from seasonal allergies, but wasn’t aware of a family history of skin disorders.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Diagnosis: Chronic atopic dermatitis

Although the patient was told she had psoriasis by previous doctors, we diagnosed her condition as atopic dermatitis based on its clinical appearance. There is no single test that can establish a diagnosis of atopic dermatitis. While serum total IgE levels are often elevated, testing is not currently recommended.

The United Kingdom working group on atopic dermatitis published diagnostic criteria based on clinical history and physical exam that include pruritic skin in addition to the presence of 3 or more of the following: skin crease involvement, chronically dry skin, symptom onset before 2 years of age, and visible evidence of dermatitis involving flexural surfaces.¹ Our patient fulfilled all but one condition, as she wasn’t sure if her symptoms began before age 2.

Approximately 70% of patients with atopic dermatitis have a positive family history of an atopic disease, such as eczema, asthma, or allergic rhinitis.

Atopic dermatitis is a chronic and inflammatory cutaneous disease that affects approximately 10% to 12% of children and less than 1% of adults in the United States.² Approximately 90% of cases present before the age of 5 and the literature demonstrates a slight female predominance.^3,4

Disease severity is classified as mild, moderate, or severe.⁵ Mild disease is characterized by dry skin and minimal itching with little impairment of the patient’s physical and psychological wellbeing. Moderate disease includes frequent pruritus and erythema with or without secondary skin changes and a moderate impact on physical and mental health. In severe disease, extensive secondary skin changes exist and the patient’s daily activities, sleep, and mental health may be severely impaired.

Etiology is multifactorial. Causes of atopic dermatitis include abnormalities in the epidermal stratum corneum and tight junctions, a heightened type-2 helper T-cell response to environmental antigens, innate immunity defects, and altered microbial skin flora.^6,7

Genetic influences appear to play a substantial role in disease development. Approximately 70% of patients have a positive family history of an atopic disease such as eczema, asthma, or allergic rhinitis.⁸ Genetic defects are believed to be related to defective proteins and lipids in the epidermis that lead to disruption of the epidermal barrier and subsequent cutaneous inflammation.^6,7

Clinical presentation: Lesion distribution varies with age

Intense pruritus and dry scaly skin occur in both children and adults, although the distribution of lesions may vary with age. Children typically exhibit erythematous patches with papules and crusting on the face, scalp, extremities, or trunk. In adults, lesions are primarily located on the hands and feet, but may also present on the face, wrists, forearms, and flexural areas.³

Adults also frequently present with secondary skin changes such as thickened skin, pigmentation changes, lichenification, and excoriated papulesdue to chronic rubbing or scratching.³ Our patient presented with significant lichenification and hyperpigmentation of the skin that was most prominent on the wrists and forearms.

Additional clinical features consistent with atopic dermatitis include a personal history of allergic conditions and a disease course characterized by exacerbations and remissions. Exacerbations may be caused by heat exposure, dry climates, anxiety, rapid temperature variations, contact with certain chemical substances, or microbial infections.⁸

Differential Dx includes psoriasis and scabies

The differential diagnosis of chronic atopic dermatitis consists of allergic or irritant contact dermatitis, plaque psoriasis, seborrheic dermatitis, scabies, and drug eruptions. Early diagnosis of atopic dermatitis is imperative to prevent sleep disturbances, chronic secondary skin changes, scarring, and the development of skin infections.

Allergic or irritant contact dermatitis is a cutaneous inflammation occurring after contact with an allergen or irritant. The lesions include erythematous, scaling areas with marked borders that are commonly pruritic. Acute cases often present with vesicles and bullae, while lichenification with cracks and fissures are common among chronic cases. Patch testing may be performed if the diagnosis is suspected.

Plaque psoriasis is characterized by areas of dry, erythematous, and well-demarcated plaques with silver scales that are most commonly found on the knees, elbows, scalp, and lower back. Systemic manifestations can include joint pain and joint swelling. Nail pitting and onycholysis are also common. While our patient had skin thickening, it was from the lichenification that is common in atopic dermatitis.

Psoriasis and atopic dermatitis are often confused. Psoriasis has discrete plaques on extensor surfaces and is often associated with nail changes, while the thickening of the skin that comes with chronic itch and scratching of atopic dermatitis is often less well circumscribed and found on flexor surfaces. Family physicians are frequently the first to encounter patients with atopic dermatitis and psoriasis and must be able to distinguish these conditions, as their treatments differ.

Seborrheic dermatitis is a chronic, relapsing inflammatory condition characterized by pruritic, erythematous, greasy, scaly patches on sebum-rich skin such as the scalp, face, and upper trunk. Seborrheic dermatitis is a clinical diagnosis.

Scabies is a pruritic skin condition caused by Sarcoptes scabiei var hominis. Characteristic linear burrows often appear as serpiginous, gray, threadlike elevations in the webbed spaces of the fingers, scrotum, areolae, elbows, axillae, feet, and wrist flexors. Secondary lesions from scratching or inflammation include excoriations, erythema, and hyperpigmentation. The diagnosis is made clinically and confirmed by dermoscopy, when available. Alternatively, mites or eggs may be observed on skin scrapings using light microscopy.

Drug eruptions should be considered in individuals taking medications who develop acute, symmetric cutaneous eruptions that may be morbilliform, urticarial, papulosquamous, pustular, or bullous in nature.

Treatment depends on severity, area of involvement, and patient’s age

Components of atopic dermatitis treatment include skin hydration, negative stimuli avoidance, pharmacologic modalities, and patient education. Improved skin hydration can be achieved by applying thick emollients containing little to no water at least twice daily and after bathing.

Topical corticosteroids are added when emollient use alone fails. Potency selection is based upon the patient’s age, involved body region, and the severity of skin inflammation.⁸ In order to reduce cutaneous atrophy, only low-potency corticosteroids should be applied to the face, groin, and axillae. Patients with mild disease may apply desonide 0.05% or hydrocortisone 2.5% cream or ointment once or twice daily for 2 to 4 weeks.⁸ Patients without improvement or with moderate disease may need medium- to high-potency steroids such as fluocinolone 0.025% or triamcinolone 0.1%.

Exacerbations of atopic dermatitis may be caused by heat exposure, anxiety, rapid temperature variations, contact with certain chemical substances, or microbial infections.

Patients with atopic dermatitis on the face, eyelids, neck, and skin folds or those who do not obtain relief from combined emollients and topical corticosteroids may benefit from topical calcineurin inhibitors such as pimecrolimus or tacrolimus.⁹ However, these agents should be utilized only for short periods of time and avoided in immunocompromised patients and those younger than 2 years of age.⁹

Patients with uncontrolled moderate to severe refractory disease may consider a trial of phototherapy or cyclosporine if phototherapy is ineffective or unavailable.¹⁰ A meta-analysis has shown that once remission is achieved, intermittent therapy with moderate- to high-potency corticosteroids or tacrolimus may be effective in reducing subsequent flares.¹¹

In all cases, sedating antihistamines such as diphenhydramine or hydroxyzine can be utilized for pruritic relief, particularly at night. Additionally, signs suggestive of infection should prompt antibiotic treatment with agents that provide coverage for Staphylococcus and Streptococcus species. Lastly, patients must be adequately educated on stimuli avoidance (eg, hot water, wool) and counseled on the medical and psychological issues that often accompany atopic dermatitis.

Our patient was placed on triamcinolone 0.1% for 4 weeks and her condition improved.

CORRESPONDENCE
Andrea Richardson, MD, MPH, 7414 Carriage Bay, San Antonio, TX 78249; [email protected].

A 30-year-old pregnant woman presented to a rural Panamanian hospital with new onset genital pain, vaginal itching, and dysuria that she’d had for 48 hours. The patient was in the first trimester of her pregnancy and indicated that she’d had recent unprotected sex with a new partner who wasn’t the father of the developing fetus. The patient had never experienced symptoms like these before and denied ever having a sexually transmitted infection (STI). On physical exam, the physician noted numerous pustules covering tender, swollen labia (FIGURE). A small amount of white discharge was noted at the introitus.

Diagnosis: Herpes simplex virus

The physician on-call diagnosed candida vaginitis along with a bacterial skin infection, and admitted the patient to the hospital for intravenous (IV) antibiotics. Fortunately, we were there on a medical mission and were consulted on the case.

We diagnosed a primary herpes simplex virus type 2 (HSV-2) infection in this patient, based on the classic presentation of grouped pustules and vesicles on erythematous and swollen labia, and the patient’s complaint of dysuria.

Herpes cultures weren’t available in the hospital, but the clinical picture was unmistakable for HSV infection. Since multiple STIs may occur simultaneously, we ordered a serum rapid plasma reagin (RPR) test for syphilis, and tested her urine for gonorrhea and chlamydia. The tests were negative.

Differential Dx includes other STIs and a fixed drug eruption

Herpes is a common STI and most people don’t have symptoms. In 2012, an estimated 417 million people worldwide were living with genital herpes caused by HSV-2.¹

The differential diagnosis for HSV infection includes primary syphilis, chancroid, folliculitis, and fixed drug eruptions.

Primary syphilis (Treponema pallidum) commonly presents with a painless, ulcerated, clean-based ulcer. While the chancre of primary syphilis can sometimes be painful, this patient did not have ulcers at the time of her presentation. Her pustules would likely ulcerate over time, but would not resemble the chancre of syphilis.

Chancroid (Haemophilus ducreyi) is a less common STI than syphilis and HSV infection. It presents with deep, sharply defined, purulent ulcers that are often associated with painful adenopathy. The ulcers can appear grey or yellowish in color.

Folliculitis presents with pustules surrounding hair follicles. Some of the pustules were surrounding hair follicles in this patient’s case, but others were independent of the hair. The patient’s marked swelling and tenderness along with dysuria also did not fit the characteristics of folliculitis.

Fixed drug eruptions can occur in the genital region, but the patient had neither bullous nor ulcerated eruptions (as one would expect with this condition). Fixed drug eruptions are usually hyperpigmented and require a history of taking medication, such as an antibiotic or a nonsteroidal anti-inflammatory drug.

Questions that help narrow the differential. Zeroing in on the cause of a patient’s genital lesions requires that you ask whether the lesions are painful, if the patient has dysuria, if there are any constitutional symptoms, and if this has happened before. Other distinguishing factors include enlarged lymph nodes and the presence of multiple (vs single) lesions.

Viral cell cultures are the preferred lab test

Antiviral therapy is most effective if begun within 72 hours of symptom onset in primary herpes genitalis.

Common laboratory tests to make the diagnosis include viral culture, direct fluorescence antibody (DFA), polymerase chain reaction (PCR), and type-specific serologic tests.

Viral cell culture is the preferred test for suspected HSV of the skin and mucous membranes.² PCR is the preferred test for suspected herpes meningitis or encephalitis when cerebrospinal fluid has been obtained through lumbar puncture.³ DFA and herpes culture can be ordered simultaneously. DFA can provide a quick result, and herpes culture can provide a more sensitive result (this may take 5-7 days before results are available).

No evidence that antivirals pose risk during pregnancy

Treatment with antivirals (acyclovir, famciclovir, or valacyclovir) may help to reduce the length of the outbreak. Oral antivirals are usually sufficient for uncomplicated HSV; IV antivirals may be needed in complicated cases. The current recommendation for acyclovir (the most commonly prescribed drug for HSV infection) is 400 mg 3 times daily or 200 mg 5 times daily for 7 to 10 days in a primary outbreak.³

Antiviral therapy is most effective if begun within 72 hours of symptom onset in primary herpes genitalis.⁴ Analgesics can help with pain control and sitz baths are helpful for women with severe dysuria.

Maternal–fetal transmission of HSV is associated with significant morbidity and mortality in children.⁵ The Centers for Disease Control and Prevention and the American College of Obstetricians and Gynecologists recommend that cesarean delivery be offered as soon as possible to women who have active HSV lesions or, in those with a history of genital herpes, symptoms of vulvar pain or burning at the time of delivery.³

There is no evidence that the use of antiviral agents in women who are pregnant and have a history of genital herpes prevents perinatal transmission of HSV to neonates.⁶ However, antenatal antiviral prophylaxis has been shown to reduce viral shedding, recurrences at delivery, and the need for cesarean delivery.⁷

Our patient was treated with oral acyclovir 400 mg 3 times a day for 10 days. One day after seeking care, she had less pain, swelling, and tenderness and was discharged. (Based on the severity of the outbreak and lack of sanitary living conditions, hospitalization was the safest and most reliable option.) The patient was counseled on the ramifications of HSV infection in pregnancy, including the fact that she might need a cesarean section. She was told that she must get prenatal care and that she needed to tell her primary care physician about her HSV infection. She was also warned about the risk of disease transmission to sexual partners and the importance of using barrier contraception to minimize the risk of future transmission.

CORRESPONDENCE
Luke Wallis, BS, 6410 Rambling Trail Drive, San Antonio, TX 78240; [email protected].

A 30-year-old pregnant woman presented to a rural Panamanian hospital with new onset genital pain, vaginal itching, and dysuria that she’d had for 48 hours. The patient was in the first trimester of her pregnancy and indicated that she’d had recent unprotected sex with a new partner who wasn’t the father of the developing fetus. The patient had never experienced symptoms like these before and denied ever having a sexually transmitted infection (STI). On physical exam, the physician noted numerous pustules covering tender, swollen labia (FIGURE). A small amount of white discharge was noted at the introitus.

Diagnosis: Herpes simplex virus

The physician on-call diagnosed candida vaginitis along with a bacterial skin infection, and admitted the patient to the hospital for intravenous (IV) antibiotics. Fortunately, we were there on a medical mission and were consulted on the case.

We diagnosed a primary herpes simplex virus type 2 (HSV-2) infection in this patient, based on the classic presentation of grouped pustules and vesicles on erythematous and swollen labia, and the patient’s complaint of dysuria.

Herpes cultures weren’t available in the hospital, but the clinical picture was unmistakable for HSV infection. Since multiple STIs may occur simultaneously, we ordered a serum rapid plasma reagin (RPR) test for syphilis, and tested her urine for gonorrhea and chlamydia. The tests were negative.

Differential Dx includes other STIs and a fixed drug eruption

Herpes is a common STI and most people don’t have symptoms. In 2012, an estimated 417 million people worldwide were living with genital herpes caused by HSV-2.¹

The differential diagnosis for HSV infection includes primary syphilis, chancroid, folliculitis, and fixed drug eruptions.

Primary syphilis (Treponema pallidum) commonly presents with a painless, ulcerated, clean-based ulcer. While the chancre of primary syphilis can sometimes be painful, this patient did not have ulcers at the time of her presentation. Her pustules would likely ulcerate over time, but would not resemble the chancre of syphilis.

Chancroid (Haemophilus ducreyi) is a less common STI than syphilis and HSV infection. It presents with deep, sharply defined, purulent ulcers that are often associated with painful adenopathy. The ulcers can appear grey or yellowish in color.

Folliculitis presents with pustules surrounding hair follicles. Some of the pustules were surrounding hair follicles in this patient’s case, but others were independent of the hair. The patient’s marked swelling and tenderness along with dysuria also did not fit the characteristics of folliculitis.

Fixed drug eruptions can occur in the genital region, but the patient had neither bullous nor ulcerated eruptions (as one would expect with this condition). Fixed drug eruptions are usually hyperpigmented and require a history of taking medication, such as an antibiotic or a nonsteroidal anti-inflammatory drug.

Questions that help narrow the differential. Zeroing in on the cause of a patient’s genital lesions requires that you ask whether the lesions are painful, if the patient has dysuria, if there are any constitutional symptoms, and if this has happened before. Other distinguishing factors include enlarged lymph nodes and the presence of multiple (vs single) lesions.

Viral cell cultures are the preferred lab test

Antiviral therapy is most effective if begun within 72 hours of symptom onset in primary herpes genitalis.

Common laboratory tests to make the diagnosis include viral culture, direct fluorescence antibody (DFA), polymerase chain reaction (PCR), and type-specific serologic tests.

Viral cell culture is the preferred test for suspected HSV of the skin and mucous membranes.² PCR is the preferred test for suspected herpes meningitis or encephalitis when cerebrospinal fluid has been obtained through lumbar puncture.³ DFA and herpes culture can be ordered simultaneously. DFA can provide a quick result, and herpes culture can provide a more sensitive result (this may take 5-7 days before results are available).

No evidence that antivirals pose risk during pregnancy

Treatment with antivirals (acyclovir, famciclovir, or valacyclovir) may help to reduce the length of the outbreak. Oral antivirals are usually sufficient for uncomplicated HSV; IV antivirals may be needed in complicated cases. The current recommendation for acyclovir (the most commonly prescribed drug for HSV infection) is 400 mg 3 times daily or 200 mg 5 times daily for 7 to 10 days in a primary outbreak.³

Antiviral therapy is most effective if begun within 72 hours of symptom onset in primary herpes genitalis.⁴ Analgesics can help with pain control and sitz baths are helpful for women with severe dysuria.

Maternal–fetal transmission of HSV is associated with significant morbidity and mortality in children.⁵ The Centers for Disease Control and Prevention and the American College of Obstetricians and Gynecologists recommend that cesarean delivery be offered as soon as possible to women who have active HSV lesions or, in those with a history of genital herpes, symptoms of vulvar pain or burning at the time of delivery.³

There is no evidence that the use of antiviral agents in women who are pregnant and have a history of genital herpes prevents perinatal transmission of HSV to neonates.⁶ However, antenatal antiviral prophylaxis has been shown to reduce viral shedding, recurrences at delivery, and the need for cesarean delivery.⁷

Our patient was treated with oral acyclovir 400 mg 3 times a day for 10 days. One day after seeking care, she had less pain, swelling, and tenderness and was discharged. (Based on the severity of the outbreak and lack of sanitary living conditions, hospitalization was the safest and most reliable option.) The patient was counseled on the ramifications of HSV infection in pregnancy, including the fact that she might need a cesarean section. She was told that she must get prenatal care and that she needed to tell her primary care physician about her HSV infection. She was also warned about the risk of disease transmission to sexual partners and the importance of using barrier contraception to minimize the risk of future transmission.

CORRESPONDENCE
Luke Wallis, BS, 6410 Rambling Trail Drive, San Antonio, TX 78240; [email protected].

A 30-year-old pregnant woman presented to a rural Panamanian hospital with new onset genital pain, vaginal itching, and dysuria that she’d had for 48 hours. The patient was in the first trimester of her pregnancy and indicated that she’d had recent unprotected sex with a new partner who wasn’t the father of the developing fetus. The patient had never experienced symptoms like these before and denied ever having a sexually transmitted infection (STI). On physical exam, the physician noted numerous pustules covering tender, swollen labia (FIGURE). A small amount of white discharge was noted at the introitus.

Diagnosis: Herpes simplex virus

The physician on-call diagnosed candida vaginitis along with a bacterial skin infection, and admitted the patient to the hospital for intravenous (IV) antibiotics. Fortunately, we were there on a medical mission and were consulted on the case.

We diagnosed a primary herpes simplex virus type 2 (HSV-2) infection in this patient, based on the classic presentation of grouped pustules and vesicles on erythematous and swollen labia, and the patient’s complaint of dysuria.

Herpes cultures weren’t available in the hospital, but the clinical picture was unmistakable for HSV infection. Since multiple STIs may occur simultaneously, we ordered a serum rapid plasma reagin (RPR) test for syphilis, and tested her urine for gonorrhea and chlamydia. The tests were negative.

Differential Dx includes other STIs and a fixed drug eruption

Herpes is a common STI and most people don’t have symptoms. In 2012, an estimated 417 million people worldwide were living with genital herpes caused by HSV-2.¹

The differential diagnosis for HSV infection includes primary syphilis, chancroid, folliculitis, and fixed drug eruptions.

Primary syphilis (Treponema pallidum) commonly presents with a painless, ulcerated, clean-based ulcer. While the chancre of primary syphilis can sometimes be painful, this patient did not have ulcers at the time of her presentation. Her pustules would likely ulcerate over time, but would not resemble the chancre of syphilis.

Chancroid (Haemophilus ducreyi) is a less common STI than syphilis and HSV infection. It presents with deep, sharply defined, purulent ulcers that are often associated with painful adenopathy. The ulcers can appear grey or yellowish in color.

Folliculitis presents with pustules surrounding hair follicles. Some of the pustules were surrounding hair follicles in this patient’s case, but others were independent of the hair. The patient’s marked swelling and tenderness along with dysuria also did not fit the characteristics of folliculitis.

Fixed drug eruptions can occur in the genital region, but the patient had neither bullous nor ulcerated eruptions (as one would expect with this condition). Fixed drug eruptions are usually hyperpigmented and require a history of taking medication, such as an antibiotic or a nonsteroidal anti-inflammatory drug.

Questions that help narrow the differential. Zeroing in on the cause of a patient’s genital lesions requires that you ask whether the lesions are painful, if the patient has dysuria, if there are any constitutional symptoms, and if this has happened before. Other distinguishing factors include enlarged lymph nodes and the presence of multiple (vs single) lesions.

Viral cell cultures are the preferred lab test

Antiviral therapy is most effective if begun within 72 hours of symptom onset in primary herpes genitalis.

Common laboratory tests to make the diagnosis include viral culture, direct fluorescence antibody (DFA), polymerase chain reaction (PCR), and type-specific serologic tests.

Viral cell culture is the preferred test for suspected HSV of the skin and mucous membranes.² PCR is the preferred test for suspected herpes meningitis or encephalitis when cerebrospinal fluid has been obtained through lumbar puncture.³ DFA and herpes culture can be ordered simultaneously. DFA can provide a quick result, and herpes culture can provide a more sensitive result (this may take 5-7 days before results are available).

No evidence that antivirals pose risk during pregnancy

Treatment with antivirals (acyclovir, famciclovir, or valacyclovir) may help to reduce the length of the outbreak. Oral antivirals are usually sufficient for uncomplicated HSV; IV antivirals may be needed in complicated cases. The current recommendation for acyclovir (the most commonly prescribed drug for HSV infection) is 400 mg 3 times daily or 200 mg 5 times daily for 7 to 10 days in a primary outbreak.³

Antiviral therapy is most effective if begun within 72 hours of symptom onset in primary herpes genitalis.⁴ Analgesics can help with pain control and sitz baths are helpful for women with severe dysuria.

Maternal–fetal transmission of HSV is associated with significant morbidity and mortality in children.⁵ The Centers for Disease Control and Prevention and the American College of Obstetricians and Gynecologists recommend that cesarean delivery be offered as soon as possible to women who have active HSV lesions or, in those with a history of genital herpes, symptoms of vulvar pain or burning at the time of delivery.³

There is no evidence that the use of antiviral agents in women who are pregnant and have a history of genital herpes prevents perinatal transmission of HSV to neonates.⁶ However, antenatal antiviral prophylaxis has been shown to reduce viral shedding, recurrences at delivery, and the need for cesarean delivery.⁷

Our patient was treated with oral acyclovir 400 mg 3 times a day for 10 days. One day after seeking care, she had less pain, swelling, and tenderness and was discharged. (Based on the severity of the outbreak and lack of sanitary living conditions, hospitalization was the safest and most reliable option.) The patient was counseled on the ramifications of HSV infection in pregnancy, including the fact that she might need a cesarean section. She was told that she must get prenatal care and that she needed to tell her primary care physician about her HSV infection. She was also warned about the risk of disease transmission to sexual partners and the importance of using barrier contraception to minimize the risk of future transmission.

CORRESPONDENCE
Luke Wallis, BS, 6410 Rambling Trail Drive, San Antonio, TX 78240; [email protected].