CHAPTER 5: ECZEMA, ATOPIC DERMATITIS, NON-INFECTIOUS IMMUNODEFICIENCY DISORDERS Flashcards
derived from the Greek word ekzein, meaning to “to boil forth” or “to effervesce.”
. . .
The acute stage generally presents as a red edematous plaque that may have grossly visible, small, grouped vesicles. Subacute lesions present as erythematous plaques with scale or crusting. Later, lesions may be covered by a drier scale or may become lichenified.
. . .
severe pruritus is a prominent symptom. The degree of irritation at which itching begins (the itch threshold) is lowered by stress. Itching is often prominent at bedtime and usually results in insomnia. Heat and sweating may also provoke episodes of itching.
eczema
What is the hallmark of all eczematous eruptions?
Histologically, the hallmark of all eczematous eruptions is a serous exudate between cells of the epidermis (spongiosis), with an underlying dermal perivascular lymphoid infiltrate and exocytosis (lymphocytes present in overlying epidermis singly or in groups).
Spongiosis is generally out of proportion to the lymphoid cells in the epidermis. This is in contrast to mycosis fungoides, which demonstrates minimal spongiosis confined to the area immediately surrounding the lymphocytes.
In most eczematous processes, spongiosis is very prominent in the acute stage, where it is accompanied by minimal acanthosis or hyperkeratosis. Subacute spongiotic dermatitis demonstrates epidermal spongiosis with acanthosis and hyperkeratosis. Chronic lesions may have minimal accompanying spongiosis, but acute and chronic stages may overlap because episodes of eczematous dermatitis follow one another. Scale corresponds to foci of parakeratosis produced by the inflamed epidermis. A crust is composed of serous exudate, acute inflammatory cells, and keratin. Eczema, regardless of cause, will manifest similar histologic changes if allowed to persist chronically. These features are related to chronic rubbing or scratching and correspond clinically to lichen simplex chronicus or prurigo nodularis. Histologic features at this stage include compact hyperkeratosis, irregular acanthosis, and thickening of the collagen bundles in the papillary portion of the dermis. The dermal infiltrate at all stages is predominantly lymphoid, but an admixture of eosinophils may be noted. Neutrophils generally appear in secondarily infected lesions. Spongiosis with many intraepidermal eosinophils may be seen in the early spongiotic phase of pemphigoid, pemphigus, and incontinentia pigmenti, as well as some cases of allergic contact dermatitis.
chronic, inflammatory skin disease characterized by pruritus and a chronic course of exacerbations and remissions
Atopic dermatitis (AD)
It is associated with other atopic conditions, including food allergies, asthma, allergic rhinoconjunctivitis, eosinophilic esophagitis, and eosinophilic gastroenteritis. Because AD usually precedes the appearance of these other atopic conditions, it has been proposed that AD is the first step in an “atopic march” whereby sensitization to allergens through the skin may lead to allergic responses in the airways or digestive tract. Although this sequence of atopic conditions does occur in many children, whether the AD is causal in the development of the other manifestations of atopy is unproved but plausible. For this reason, early and effective treatment of AD is encouraged in an effort to prevent other atopic conditions. The genetic defect(s) predisposing at-risk individuals to the development of AD is the same for asthma and allergic rhinoconjunctivitis, and thus it has been difficult to prove that AD is causal in the development of other atopic conditions.
3 stages of AD
AD can be divided into three stages:
- infantile AD, occurring from 2 months to 2 years of age;
- childhood AD, from 2–10 years; and
- adolescent/adult AD.
What are the clinical manifestations of AD?
In all stages, pruritus is the hallmark. Itching often precedes the appearance of lesions, thus the concept that AD is “the itch that rashes.” Useful diagnostic criteria include those of Hannifin and Rajka, the UK Working Party, and the American Academy of Dermatology’s Consensus Conference on Pediatric Atopic Dermatitis (Boxes 5 1 and 5.2). These criteria have specificity at or above 90% but have much lower sensitivities (40%–100%). Therefore these criteria are useful for enrolling patients in studies and ensuring that they have AD, but less practical in diagnosing a specific patient with AD.
Hannifin and Rajka Criteria for Atopic Dermatitis
MNEMONIC : CHIP BAKES DRIP
MAJOR CRITERIA ( atleast 3):
Mnemonic : CHIP
C-hronicity
H-/O Atopy (Personal/Family)
I-nvolvement of Face & Flexures (Popliteal & Antecubital fossa)
P-ruritis
MINOR CRITERIA (atleast 3)
Mnemonic: BAKES DRIP
Delayed Blanching to Cholinergics
Anterior Subcapsular Cataract
Keratoconus
Raised IgE
Immediate (Type 1)** S**kin Test
D-ennie’s I ines
R-ecurrent skin infections
I-cthvosis Vulgaris over palmar crease
Facial Pallor
. . .
BOX 5.1 Criteria for Atopic Dermatitis
MAJOR CRITERIA
Must have three of the following:
1. Pruritus
2. Typical morphology and distribution
Flexural lichenification in adults,
Facial and extensor involvement in infancy
3. Chronic or chronically relapsing dermatitis
4. Personal or family history of atopic disease (e.g., asthma,
allergic rhinitis, atopic dermatitis)
MINOR CRITERIA
Must also have three of the following:
1. Xerosis
2. Ichthyosis/hyperlinear palms/keratosis pilaris
3. IgE reactivity (immediate skin test reactivity, RAST test
positive)
4 .Elevated serum lgE
5.Early age of onset
6. Tendency for cutaneous infections (especially Staphylococcus
aureus and HSV)
7. Tendency to nonspecific hand/foot dermatitis
8. Nipple eczema
9. Cheilitis
10. Recurrent conjunctivitis
11. Dennie-Morgan infraorbital fold
12. Keratoconus
13. Anterior subcapsular cataracts
14. Orbital darkening
15. Facial pallor/facial erythema
16. Pityriasis alba
17. Itch when sweating
18 Intolerance to wool and lipid solvents
19. Perifollicular accentuation
20. Food hypersensitivity
21. Course influenced by environmental and/or emotional factors
22. White dermatographism or delayed blanch to cholinergic
agents
Modified Criteria for Children With Atopic Dermatitis
Box 5-2 Modified criteria for children with atopic dermatitis
Essential features
- Pruritus
- Eczema
* Typical morphology and age-specific pattern
* Chronic or relapsing history
Important features - Early age at onset
- Atopy
- Personal and/or family history
- IgE reactivity
- Xerosis
Associated features - Atypical vascular responses (e.g., facial pallor, white
dermatographism) - Keratosis pilaris/ichthyosis/hyperlinear palms
- Orbital/periorbital changes
- Other regional findings (e.g., perioral changes/periauricular
lesions) - Perifollicular accentuation/lichenification/prurigo lesions
present in the first year of life, but usually not until after 2 months.
. . .
children under 2 months may be from an irritant, ichthyosis, or a hallmark of severe immunodeficiency.
. . .
usually begins as erythema and scaling of the cheeks (Fig. 5.1). The eruption may extend to the scalp, neck, forehead, wrists, extensor extremities, and buttocks. There can be overlap with seborrheic dermatitis on the scalp and in the folds, but papular or nodular involvement in the ax llae and inguinal folds is more typical of scabies infestation.
. . . therapeutic effects of ultrav olet (UV) B light and humidity in many patients, as well as the aggravation by wool and dry air in the winter.
Infantile Atopic Dermatitis
During childhood, lesions tend to be less exudative. The classic locations are the antecubital and popliteal fossae (Fig. 5.2), flexor wrists, ankles, eyelids, face, and around the neck. Lesions are often lichenified, indurated plaques.
These are intermingled with isolated, excoriated, 2–4 mm papules that are scattered more widely over the uncovered parts. Nummular morphology and involvement of the feet are more common in childhood
Pruritus is a constant feature, and most of the cutaneous changes are secondary to it. Itching is paroxysmal. Scratching induces lichenification and may lead to secondary infection. A vicious cycle may be established, the itch-scratch cycle, as pruritus leads o scratching, and scratching causes secondary changes that in them cause itching. Instead of scratching causing pain, in the atopic patient the “pain” induced by scratching is perceived as itch and induces more scratching. The scratching impulse is beyond the control of the patient. Severe bouts of scratching occur during
sleep, leading to poor rest and chronic tiredness in atopic children. This can affect school performance. Parents often scold children who are scratching, and this leads to more anxiety and thus more scratching.
Severe AD involving a large percentage of the body surface area BSA) can be associated with growth retardation (Fig. 5.3). Restriction diets and steroid use may exacerbate growth impairment. Aggressive management of such children with phototherapy or systemic immunosuppressive agents may allow for rebound growth. Children with severe AD may also have substantial psychological disturbances. Parents should be questioned with regard to school performance and socialization. Although using light therapy and systemic immunosuppressive or immunomodulatory therapy in children can be daunting for patients and practitioners, the benefits to quality of life can dramatically outweigh the risks.
Fig. 5.3 Severe, widespread atopic dermatitis.
Childhood Atopic Dermatitis
**
Fig. 5.2 Flexural involvement in childhood atopic dermatitis.
Most adolescents and adults with AD will give a history of childhood disease. AD will begin after age 18 years in only 6%–14% of patients diagnosed with AD. One exception is the patient who moves from a humid, tropical region to a more temperate area of higher latitude. This climatic change is often associated with the appearance of AD. In older patients, AD may occur as localized erythematous, scaly, papular, exudative, or lichenified plaques. In adolescents, the eruption often involves the classic antecubital and popliteal fossae, front and sides of the neck, forehead, and area around the eyes. In older adults, the distribution is generally less characteristic, and localized dermatitis may be the predominant feature, especially hand, nipple, or eyelid eczema. At times, the eruption may generalize, with accentuation in the flexures. The skin generally is dry and somewhat erythematous. Lichenification and prurigo-like papules are common (Fig. 5.4). Papular lesions tend to be dry, slightly elevated, and flat topped. They are almost always excoriated and often coalesce to form plaques. Staphylococcal colonization is common. In darker-skinned patients, the lesions are often hyperpigmented, frequently with focal hypopigmented areas related to healed excoriations.
Itching usually occurs in crises or paroxysms. Adults frequently complain that flares of AD are triggered by acute emotional upsets. Stress, anxiety, and depression reduce the threshold at which itch is perceived and result in damage to the epidermal permeability barrier, further exacerbating AD. Atopic persons may sweat poorly and may complain of severe pruritus related to heat or exercise. Physical conditioning and liberal use of emollients improve this component, and atopic patients can participate in competitive sports.
Even in patients with AD in adolescence or early adulthood, improvement usually occurs over time, and dermatitis is uncommon after middle life. In general, these patients retain mild stigmata of the disease, such as dry skin, easy skin irritation, and itching in response to heat and perspiration. They remain susceptible to a flare of their disease when exposed to a specific allergen or environmental situation. Photosensitivity develops in approximately 3% of AD patients and may manifest as either a polymorphous light eruption–type reaction or simply exacerbation of the AD by UV exposure. The average age for photosensitive AD is the middle to late thirties. Human immunodeficiency virus (HIV) infection can also serve as a trigger, and new-onset AD in an at-risk adult should lead to counseling and testing for HIV if warranted.
The hands, including the wrists, are frequently involved in adults, and hand dermatitis is a common problem for adults with a history of AD. It is common for irritant or atopic hand dermatitis to appear in young women after the birth of a child, when increased exposure to soaps and water triggers their disease. There is a new trend in children who can buy kits or mix their own various household liquids such as glue, borax, contact solution, baking soda and others to make “slime” This can lead to irritant dermatitis or worsening of hand atopic dermatitis. Wet work is a major factor in hand eczema in general, including those patients with AD.
Atopic Dermatitis in Adolescents and Adults
Fig. 5.4 Prurigo-like papules in adult atopic dermatitis.
can affect both the dorsal and the palmar surface (Fig. 5.5). Keratosis punctata of the creases, a disorder seen almost exclusively in black persons, is also more common in atopic patients. Patients with AD have frequent exposure to preservatives and other potential allergens in the creams and lotions that are continually applied to their skin. Contact allergy may manifest as chronic hand eczema. Patch testing can help differentiate an allergic contact dermatitis.
Fig. 5.5 Atopic hand dermatitis.
Eyelids are often involved (Fig. 5.6). In general, the involvement is bilateral and the condition flares with cold weather. As in hand dermatitis, irritants and allergic contact allergens must be excluded by a careful history and patch testing.
Fig. 5.6 Periocular atopic dermatitis.
linear transverse fold just below the edge of the lower eyelids
**Dennie-Morgan fold **- indicative of the atopic diathesis, although it may be seen with any chronic dermatitis of the lower lids
In atopic patients with eyelid dermatitis, increased folds and darkening under the eyes is common.
When there is extensive facial involvement, the nose is still typically spared. This is called the ______
“headlight sign.”
The axillary vault and inguinal folds are also typically spared likely due to high humidity in these areas.
Other manifestations of AD
The less involved skin of atopic patients is frequently dry and slightly erythematous and may be scaly. Histologically, the apparently normal skin of atopic patients is frequently inflamed subclinically. The dry, scaling skin of AD may represent low-grade dermatitis. Pityriasis alba is a form of subclinical dermatitis, frequently atopic in origin. It presents as poorly marginated, hypopigmented, slightly scaly patches on the cheeks, upper arms, and trunk, typically in children and young adults with types III to V skin. It usually responds to emollients and mild topical steroids, preferably in an ointment base.
consists of horny follicular lesions of the outer aspects of the upper arms, legs, cheeks, and buttocks and is often associated with AD, AD and occurs in patients with filagrin mutations.
Keratosis pilaris (KP)
The keratotic papules on the face may be on a red background, a variant of KP called keratosis pilaris rubra faceii.
KP is often refractory to treatment. Moisturizers alone are only partially beneficial. Some patients will respond to topical lactic acid, urea, or retinoids but they can easily irritate the skin of atopic patients and should be avoided in young children. If older patients desire, treatment should begin with applications only once or twice a week. KP must be differentiated from follicular eczema which tends to affect the trunk and is often more prominent in patients with skin ypes III-VI.
Thinning of the lateral eyebrows is sometimes present in AD
Hertoghe sign
This apparently occurs from chronic rubbing caused by pruritus and subclinical dermatitis. Hyperkeratos s and hyperpigmentation, which produce a “dirty neck” appearance, are also common in AD patients.
blanching of the skin at the site of stroking or scratching
White dermatographism
Chronic exposure to the vasoconstrictive effects of topical and oral steroids may lead to erythroderma due to vasodilation when steroids are tapered. This can lead to dysesthesias and belies the importance of using maintenance therapies that limit steroid exposure or lessen strength.
Ophthalmologic Abnormalities in AD
Up to 10% of patients with AD develop cataracts, either anterior or posterior subcapsular. Posterior subcapsular cataracts in atopic individuals are indistinguishable from corticosteroid-induced cataracts. Development of cataracts is more common in patients with severe dermatitis. Keratoconus is an uncommon finding, occurring in approximately 1% of atopic patients. Contact lenses, keratoplasty, and intraocular lenses may be required to treat this condition. Environmental allergies may also lead to allergic rhinoconjunctivitis.
Give diferential diagnosis for AD
- Typical AD in infancy and childhood is straightforward because of its characteristic morphology; predilection for symmetric involvement of the face, neck, and antecubital and popliteal fossae; and association with food allergy, asthma, and allergic rhinoconjunctivitis.
- Dermatoses that may resemble AD include seborrheic dermatitis (especially in infants), irritant or allergic contact dermatitis, nummular dermatitis, photodermatitis, scabies, and cases of psoriasis with an eczematous morphology.
- Certain immunodeficiency syndromes (see later discussion) may exhibit a dermatitis remarkably similar or identical to AD.
- In older patients with new onset dermatitis, cutaneous T cell lymphoma and allergic contact dermatitis should be considered.
Histopathologic findings of AD
The histology of AD varies with the stage of the lesion, with many of the changes induced by scratching. Hyperkeratosis, acanthosis, and excoriation are common
Staphylococcal colonization may be noted histologically. Although eosinophils may not be seen in the dermal infiltrate, staining for eosinophil major basic protein (MBP) reveals deposition in many cases.
Antipruritic therapy for AD
The primary treatment for the pruritus of AD is to reduce the severity of the AD.
Antihistamines are frequently used for the pruritus of AD but are mainly beneficial for their sedative properties:
- long-acting histamine-2 blockers such as cetirizine, loratadine, and fexofenadine may help by decreasing the symptoms of the environmental allergies.
- Diphenhydramine, hydroxyzine, and doxepin can all be efficacious. Nonsedating antihistamines do not appear to benefit the pruritus of AD in standard doses.
- In some patients, gabapentin, selective serotonin reuptake inhibitors (SSRIs), mirtazapine, and even opiate antagonists may reduce pruritus.
- Applying ice during intense bouts of itch may help to “break” an itch paroxysm.
Moisturizing lotions containing menthol, phenol, or pramoxine can be used between steroid applications to moisturize and reduce local areas of severe itch. More widespread use of topical doxepin (Sinequan) is limited by systemic absorption and sedation.
most common class of medications, along with moisturizers, used for the treatment of AD
Topical corticosteroids
. . .
They are effective and economical. Ointments are preferred because they can serve a do ble purpose as an emollient, they do not burn when applied, and they typically have fewer ingredients leading to lower of a chance of allergic contact dermatitis
In infants, low-potency steroid ointments, are preferred. Regular application of emollients must be emphasized Once corticosteroid receptors are saturated, additional applications of a steroid preparation contribute nothing more than an emollient effect. In most body sites, once-daily application of a corticosteroid is almost as effective as more frequent applications, at lower cost and with less systemic absorption and likely increased compliance. In some areas, twice-daily applications may be beneficial, but more frequent applications are almost never of benefit.
Application of topical corticosteroids under wet wraps or vinyl suit occlusion especially after soaking in a tub of water (soak and smear) can increase efficiency.
In refractory and relapsing AD, twice-weekly steroid application to the areas that commonly flare may reduce flares. Another maintenance method is to mix 1 part of hydrocortisone 2.5% ointment in with 1 to 4 parts of the patient’s preferred emollient 2–5 days per week, lessening the amount this is used as tolerated.
In older children and adults, medium-potency steroids are often used, except on the face, where milder steroids or calcineurin inhibitors are preferred. For thick plaques and lichen simplex chronicus–like lesions, extremely potent steroids may be necessary.
Ideally prevention of AD flares is with just emollients, but patients with more severe disease often need some consistent antiinflammatory medicines (similar to the paradigm used for asthma). Maintenance therapy with topical steroids as discussed earlier can be with twice-weekly application, mixing a low-potency steroid in with an emollient or with nonsteroidal antiinflammatory medications.
examples of Topical Calcineurin Inhibitors for AD
Topical calcineurin inhibitors (TCIs) such as t**acrolimus or pimecrolimus **offer an alternative to topical steroids. Systemic absorption is generally not significant with either of these agents.
Although a 0.03% tacrolimus ointment is marketed for use in children, it is unclear whether it really offers any safety advantage over the 0.1% formulation. Patients may experience a warm or stinging feeling in the skin when the medicines are first started. This tends to resolve and tolerability is improved if the ointment is applied to “bone-dry” skin Patients experience less burning if eczematous patches are treated initially with a corticosteroid, with transition to a TCI after partial clearing. Improvement tends to be steady, with progressively smaller areas requiring treatment. TCIs are particularly useful on the eyelids and face, in areas prone to steroid atrophy, when steroid allergy is a consideration, or when systemic steroid absorption is a concern. Tacrolimus is more effective than pimecrolimus, with tacrolimus 0.1% ointment equivalent to triamcinolone acetonide 0.1%, and pimecrolimus equivalent to a class V or VI topical corticosteroid. There is a black box warning on calcineurin inhibitors in the United States, but a recent study that followed patients after marketing found no increase in malignancy in over 26,000 patient-years studied.
an antiinflammatory topical PDE4 inhibitor introduced in 2017 for AD in children over 2 years.
Crisaborole
It can be used on the face and skinfolds without concern for striae but may sting when applied. It may be most useful as a maintenance medication or for mild to moderate disease.
ex. of Tar for AD
Crude coal tar 1%–5% in white petrolatum or hydrophilic ointment USP, or liquor carbonis detergens (LCDs) 5%–20% in hydrophilic ointment USP, is sometimes helpful for an area of refractory AD.
Tar preparations are especially beneficial when used for intensive treatment for adults in an inpatient or day care setting, especially in combination with UV phototherapy.
**Goeckerman therapy with tar and UVB **in a day treatment setting will lead to improvement in more than 90% of patients with refractory AD, and prolonged remission can be induced.
Phototherapy for AD
If topical modalities fail to control AD, phototherapy is another step on the therapeutic ladder. **Narrow-band (NB) UVB **is highly effective and has replaced broadband UV for treating AD. When acutely inflamed, AD patients may tolerate UV poorly. Initial treatment with soak and smear topical steroids or a systemic immunosuppressive may cool off the skin enough to institute UV treatments.
Patients with significant erythema must be introduced to** UV at very low doses **to avoid nonspecific irritancy and flaring of the AD. Often, the initial dose is much lower and the dose escalation much slower than in patients with psoriasis. In acute flares of AD, UVA I can be used.
For patients unresponsive to NB UVB, photochemotherapy with psoralen plus UVA (PUVA) can be effective but the benefits must outweigh the risks. It requires less frequent treatments, and can be given either** topically (soak/ bath PUVA) or systemically (oral PUVA).**
an IL-4 receptor inhibitor that thus blocks the function of IL-4 and IL-13.
**dumpilumab **
…
its an injection given 2x a wk after a loading dose and decreases prutitus and eczema area and severity index (EASI) scores.
its the first targeted systemic therapy for AD.
Most common side effect is Keratoconjunctivitis.
Systemic corticosteroids in AD
In general, systemic corticosteroids should be used only to control acute exacerbations. In patients requiring systemic steroid therapy, **short courses (≤3 weeks) **are preferred. If repeated or prolonged courses of systemic corticosteroids are required to control the AD, phototherapy or a steroid-sparing agent should be considered.
Chronic corticosteroid therapy for AD frequently results in significant steroid-induced side effects. Osteoporosis in women requires special consideration and should be addressed with a **bisphosphonate **early in the course of therapy when bone loss is greatest. Preventive strate- gies, such as calcium supplements, vitamin D supplementa- tion, bisphosphonates, regular exercise, and smoking cessation, should be strongly encouraged. Dual-energy x-ray absorpti- ometry (DEXA) scans are recommended.
Cyclosporine for AD
**Cyclosporine (cyclosporin A) **is highly effective in the treat- ment of severe AD, but the response is rarely sustained after the drug is discontinued. It is very useful to gain rapid control of severe AD. Cyclosporine has been shown to be safe and effective in both children and adults, although probably toler- ated better in children. Potential long-term side effects, espe- cially renal disease, require careful monitoring, with attempts to transition the patient to a potentially less toxic agent if pos- sible. The dose range is 3–5 mg/kg in children and 150–300 mgin adults, with a better and more rapid response at the higher end of the dose range. Rebound flaring of AD is possible and can be significant after stopping cyclosporin A, and a plan should be in place for this eventuality.
methotrexate for AD
0.3- 0.6 mg/kg given once a wk ( up to 25 kg) in children and 10-25 mg weekly in adults.
give FOLIC ACID as welll
Other Immunosuppressive Agents for AD
- azathioprine (Imuran), mycophe- nolate mofetil (CellCept), and methotrexate (Rheumatrex).
- Mycophenolate mofetil (MMF)
- Low-dose weekly methotrexate
- Hydroxyurea, as used for psoriasis in the past, can be effec- tive in AD if other steroid-sparing agents fail
- Intravenous immune globulin (IVIG
- Interferon (IFN)–γ
- Traditional Chinese herb mixtures have shown efficacy in children and in animal models for AD. The active herbs appear to be ophiopogon tuber and Schisandra fruit. Chinese herbs are usually delivered as a brewed tea to be drunk daily.
may involve the helix, postauricular fold, and external auditory canal. By far the most frequently affected site is the external canal, where eczema is often a manifestation of seborrheic dermatitis or allergic contact dermatitis caused by topical medications, especially neomycin (Fig. 5-8).
**Fig. 5 8 Ear eczema or otitis externa **
. . .
Secretions of the ear canal derive from the specialized apocrine and sebaceous glands, which form cerumen. Rubbing, wiping, scratching, and picking exacerbate the condition. Secondary bacterial colonization or infection is common. Infection is usually caused by staphylococci, strep- tococci, or Pseudomonas. Contact dermatitis from neomycin, benzocaine, and preservatives may be caused by topical
Fig. 5-8 Ear eczema secondary to allergic contact dermatitis.
remedies. Pseudomonas aeruginosa can result in malignant external otitis with ulceration and sepsis. Earlobe dermatitis is virtually pathognomonic of metal contact dermatitis (espe- cially nickel) and occurs most frequently in women who have pierced ears.
Treatment should be directed at removal of causative agents, such as topically applied allergens. First, examine the ear with an otoscope and be sure there is not a perforated tympanic membrane. If there is drainage from a perforated tympanic membrane, management should be in consultation with an otolaryngologist. This purulent fluid can be the cause of an ear eczema—infectious eczematoid dermatitis. If the tympanic membrane is intact, scales and cerumen should be removed by gentle lavage with an ear syringe. A combination of cipro- floxacin plus a topical steroid (e.g., Ciprodex) is preferred to neomycin-containing products. Corticosteroids alone can be effective for noninfected dermatitis. For very weepy lesions, aluminum acetate optic solution (e.g., Domeboro) may be drying and beneficial.
usually affects the areolae and may extend on to the surrounding skin (Fig. 5-9). The area around the base of the nipple is usually spared, and the nipple itself is less frequently affected.
moist type with oozing and crusting
Breast eczema (nipple eczema)
. . .
Atopic dermatitis is a frequent cause, and nipple eczema may be the sole manifestation of AD in adult women. It frequently presents during breastfeeding. The role of secondary infection with bacteria and Candida should be considered in breastfeeding women. Other causes of nipple eczema are allergic contact dermatitis and irritant dermatitis. Irritant dermatitis occurs from friction (jogger’s nipples), or from poorly fitting brassieres with seams in women with asymmetric and large breasts. In patients in whom eczema of the nipple or areola has persisted for more than 3 months, especially if it is unilateral, a biopsy is mandatory to rule out the possibility of Paget’s disease of the breast.
Management of Breast eczema (nipple eczema)
Therapy with topical or systemic antifun- gal agents may be required to determine whether Candida is pathogenic. Oral fluconazole can be dramatically effective in these patients. Topical gentian violet 0.5%, applied once daily to the nipple for up to 1 week, or all-purpose nipple ointment (mupirocin 2%, 10 g; nystatin, 100,000 units/mL ointment, 10 g; clotrimazole 10% vaginal cream, 10 g; and betametha- sone 0.1% ointment, 10 g) is an effective topical agent. Guaia- zulene (Azulon) is a dark-blue hydrocarbon used in Europe for nipple “cracks” with breastfeeding.
The child’s thrush should also be treated. A lactation con- sultant or nurse may be helpful in managing these patients, since poor positioning during breastfeeding is a common cofactor in the development of nipple eczema.
What are the different types of eczema?
The different types of hand eczema are as follows:
1. Allergic contact dermatitis (with or without an additional irritant component)
2. Irritant hand dermatitis
3. Atopic hand eczema (with or without an additional
irritant component)
4. Recurrent vesicular (or vesiculobullous) hand eczema
5. Hyperkeratotic hand eczema
6. Pulpitis (chronic fingertip dermatitis)
7. Nummular dermatitis
