Abstract
Pustules are collections of neutrophils that are situated superficially, usually in a hair follicle (e.g., acne and folliculitis) or just below the stratum corneum (e.g., impetigo and candidiasis). Although pustules represent the unifying clinical feature of these disorders, they may not always be the predominant finding; sometimes, they are not even present. For example, in some patients with acne, only comedones or papules are found. In impetigo, often only crusts are found because the pustules have been broken and dried. Pus often indicates infection. For pustules (and crusts) in the skin, infection is an appropriate diagnostic consideration, but, as can be seen from Table 12.1 , not all pustular dermatoses are caused by pathogenic microorganisms. However, if infection is suspected, simple laboratory tests can be performed for confirmation.
The most common pustular diseases are listed in Table 12.1 . Other rare causes of pustules are mentioned briefly at the end of the chapter.
Acne
- 1.
Acne is the most common dermatologic disease with negative psychosocial ramifications
- 2.
Comedones are the hallmark of the disease
- 3.
Treatment targets multifactorial causes of acne: androgens, follicular obstruction, and Propionibacterium acnes
| Physical Examination | ||||||
|---|---|---|---|---|---|---|
| Frequency (%) a | Etiology | Appearance of Lesions | Distribution | Differential Diagnosis | Laboratory Test | |
| Acne | 13 | Multifactorial | Pustules, papules, nodules, and comedones | Face and upper trunk | Folliculitis Rosacea | None |
| Candidiasis | 0.3 | Infection ( C. albicans ) | Satellite pustules around a “ beefy red ” erythematous area | Moist areas, particularly the groin | Tinea cruris Intertrigo Miliaria Folliculitis Contact dermatitis | Potassium hydroxide preparation |
| Folliculitis | 1.1 | Infection ( S. aureus ) | Scattered pustules, many with centrally placed hairs | Buttocks and thighs, beard area, scalp | Acne Fungal infection Keratois pilaris Pseudofolliculitis | Gram-stain Culture |
| Impetigo | 0.6 | Infection ( S. aureus ) | Crusts (often honey-colored) predominant | Anywhere, most common on face | Ecthyma Herpes simplex | Gram-stain Culture |
| Rosacea | 1.3 | Unknown | Papules and pustules on a background of erythema and telangiectasia | Central portion of face | Acne Lupus erythematosus Seborrheic dermatitis | None |
a Percentage of new dermatology patients with this diagnosis seen in the Hershey Medical Center Dermatology Clinic, Hershey, PA.
Definition
Acne vulgaris (common acne) is a disorder affecting pilosebaceous units in the skin ( Fig. 12.1 ). The cause is multifactorial. Clinical lesions range from noninflamed comedones to inflammatory papules , pustules , and nodules .
Incidence
Acne is the most common disease seen by a dermatologist. It begins at a surprisingly young age; comedones can be found on examination in 50% of boys aged 9 to 11 years. Acne is a physically and psychologically devastating condition and must be treated aggressively. The incidence and severity of the disease increase during the teenage years and early adulthood, affecting approximately 85% of young people between the ages of 12 and 24 years. Contrary to popular belief, acne is not confined to teenagers. It may continue into the third and fourth decades of life, especially in women; in some patients, it does not begin until then.
History
The patient usually makes the diagnosis and often has attempted therapy with over-the-counter medication. A history of hirsutism, hair thinning usually localized to top of the scalp, or irregular menses in a woman with acne should lead to the consideration of possible androgen excess. Adult women often complain of acne along the jawline that worsens around the time of their period ( Fig. 12.2 ). For any ethnicity with darker skin, acne can lead to marks of postinflammatory hyperpigmentation, which can take many months to resolve. Topical or systemic corticosteroids can also cause an acneiform eruption.
Physical Examination
The noninflamed lesions in acne are called comedones and are of two types: (1) the open comedone or “blackhead,” which appears as a dilated pore filled with black keratinous material (not dirt); and (2) the closed comedone or “whitehead,” which is a small, flesh-colored, dome-shaped papule that often is difficult to see ( Fig. 12.3 ). Inflammatory acne lesions are seen more easily by both patient and physician. They appear as papules, pustules, or nodules, depending on the magnitude of the inflammatory response ( Fig. 12.4 ) . Acne is found in areas with numerous sebaceous glands, usually the face and upper trunk. The lower trunk is less often involved, and the distal extremities are always spared.
Noninflammatory lesions:
- 1.
Open comedones
- 2.
Closed comedones
Inflammatory lesions:
- 1.
Papules
- 2.
Pustules
- 3.
Nodules
Differential Diagnosis
The diagnosis of acne is rarely difficult, particularly in teenagers. Occasionally, acne comedones may be confused with flat warts , which are small, flesh-colored, flat-topped papules usually located on the face. On close inspection, the flat wart is seen to have a sharp right-angled edge and a finely textured surface, whereas a closed comedone has a dome-shaped, smooth surface ( Fig. 12.5 ).
Steroid acne is caused by use of corticosteroids and is distinguished from acne vulgaris by its sudden onset (usually within 2 weeks of starting high-dose systemic or potent topical corticosteroid therapy) and appearance (uniform, 2- to 3-mm, red, firm papules and pustules) ( Fig. 12.6 ). Steroid acne caused by topically applied agents occurs most often on the face. With systemic corticosteroids, the eruption is most prominent on the upper trunk.
Pustular acne vulgaris can be confused with bacterial folliculitis or rosacea. In bacterial folliculitis , hairs are visible in some of the pustules and a bacterial culture is positive, usually for Staphylococcus aureus or, less often, a Gram-negative organism. Rosacea is distinguished from acne vulgaris by the presence of a background blush of erythema and telangiectasia, and the absence of comedones. Rosacea also usually occurs later in life.
Papular acne is occasionally confused with angiofibromas and keratosis pilaris.
Angiofibromas, a skin manifestation of tuberous sclerosis, are often incorrectly diagnosed as acne. Clinically, the lesions appear as firm, pink papules that are clustered primarily in the center of the face, are persistent, and are, of course, resistant to acne therapy. Keratosis pilaris, when it affects the facial cheeks, is distinguished from acne by its minute, rough, uniform papules on the background of “red” (e.g., prominent skin vasculature) skin and by its lack of comedones. Keratosis pilaris is a chronic condition and relatively unresponsive to acne treatments.
- ●
Flat warts
- ●
Steroid acne
- ●
Folliculitis
- ●
Rosacea
- ●
Angiofibromas in tuberous sclerosis
- ●
Keratosis pilaris
Laboratory and Biopsy
The diagnosis is almost always made clinically. Occasionally, a bacterial culture is indicated to rule out infection. A biopsy is not indicated but would show an occluded pilosebaceous unit along with inflammation ( Fig. 12.7 ).
Therapy
Four categories of medication have proved efficacious in the treatment of acne: topical agents, systemic antibiotics, systemic retinoids, and hormonal agents. The type of acne guides the choice of treatment. For the majority of patients, systemic retinoids and hormonal therapy are not required.
Initial
Comedonal
- ●
Topical retinoids (tretinoin 0.05% cream in PM)
Papules and Pustules
- ●
Topical: retinoid in PM and benzoyl peroxide (alone or in combination with topical clindamycin) in AM
- ●
Systemic: tetracyclines (add if topicals fail)
Nodules
- ●
Topical and systemic therapy in combination as outlined for papules and pustules
Alternative
Comedonal
- ●
Topical adapalene (for sensitive skin)
- ●
Topical tazarotene (for resistant comedones)
Papules and Pustules
- ●
Oral isotretinoin if severe and fails initial treatment
Nodules
- ●
Oral isotretinoin
Hormonal Treatment for Females
- ●
Oral contraceptives
- ●
Spironolactone
Topical agents
Topical agents are most effective for superficial lesions. For comedones, the mainstay of treatment remains topical retinoids: tretinoin (Retin-A Micro cream), adapalene (Differin cream), and tazarotene (Tazorac). Benzoyl peroxide has mild comedolytic activity and also exerts an antibacterial effect. Topical antibiotics (erythromycin, clindamycin) should be used in combination with topical benzoyl peroxide in order to prevent bacterial resistance.
The authors usually start treatment with a topical retinoid at bedtime and a benzoyl peroxide wash (available over the counter) in the morning. The patient should apply these medications to the entire affected area (e.g., the entire face) rather than just to the individual lesions. In addition, patients must be advised that retinoids and benzoyl peroxide preparations can cause skin irritation, which usually is worst during the first 1 to 2 weeks of use and afterward diminishes. In part because of the irritation, the patient may notice that the condition appears worse rather than better after the first several weeks of use.
Systemic antibiotics
Systemic antibiotics are indicated in patients with inflammatory papules or pustules, especially if there is truncal involvement. Doxycycline (50–100 mg twice daily) is the most commonly prescribed oral antibiotic because of efficacy and relative safety. Tetracycline (500 mg twice daily) is less commonly prescribed. The authors try to limit systemic antibiotic use to no more than three months; if no improvement, then consider referral to a dermatologist. To promote compliance, the authors recommend taking tetracyclines with food and even dairy products, despite package insert recommendations. Minocycline (100 mg twice daily) is used mostly in persons who cannot tolerate the other tetracyclines.
Systemic retinoids
The oral retinoid isotretinoin became available commercially in September 1982 for use in the treatment of patients with severe acne ( Fig. 12.8 ). This potent vitamin A analog decreases follicular keratinization, sebum production, and intrafollicular bacterial counts. Side-effects are common. Almost all patients experience chapped lips and dry skin, and extracutaneous complications also occur; for example, increased levels of liver enzymes and plasma lipids. Most importantly, systemic retinoids are teratogenic . It is mandatory that female patients not be pregnant when taking isotretinoin. Special consent forms, strict birth control measures, and monthly pregnancy tests are required for women taking isotretinoin. A consent form acknowledging the risk of depression and suicide while on isotretinoin is required for both men and women. There is also a controversial link of isotretinoin to inflammatory bowel disease. Because of these restrictions, the drug is recommended mainly for the treatment of selected patients with severe, therapy-resistant papular/pustular acne or scarring nodular acne ( Fig. 12.9 ). The drug should be prescribed only by physicians who are familiar with its use and participate in a national risk management program ( www.ipledgeprogram.com ).
Isotretinoin is teratogenic.
Hormonal therapy
This class of treatment can help females who have acne that fails to respond to initial treatment outlined above and that flares with their menstrual cycle. Birth control pills with low androgenicity improve acne in many patients. Several products are available, including Ortho Tri-Cyclen and Estrostep, for which the US Food and Drug Administration has approved acne as an indicated use.
Antiandrogens have also been used for treating therapy-resistant acne in women. Cyproterone acetate is available in Europe, whereas spironolactone has been used in the United States. Again, these agents should be prescribed only by physicians who are fully aware of their potential side-effects.
Patient education
The most important aspect of a successful acne treatment program is patient compliance. Instructions should be given both verbally at the time of the patienťs initial visit and on a written take-home sheet that reinforces what was said. Patients are best able to comply if medications are used only twice daily, so that the medication schedule can be centered on an already established daily habit such as teeth brushing. At the time of the initial visit, answers can also be given to several common questions (often unasked) that patients with acne or their parents frequently have regarding the following:
- 1.
Diet . Some evidence indicates that a “Western” diet may have an adverse effect on acne, but specific foods have not been implicated. For most patients, a sensible diet is all that is suggested.
- 2.
Cleanliness . Acne is not a function of poor hygiene. In general, acne cleansing agents are also not recommended because they cause irritation that unnecessarily compounds the irritation from the recommended topical comedolytics. Instruct patients to wash their face with their hands and not with a washcloth.
- 3.
Cosmetics . If cosmetics are used, they should be water-based and used sparingly. Most cosmetic products are noncomedogenic.
- 4.
Picking . In many patients with acne, much of the skin damage is self-inflicted. Although the temptation to squeeze a fresh pustule is often overwhelming, it should be vigorously discouraged because it can produce more tissue damage, sometimes resulting in post-inflammatory hyperpigmentation and scars.
- 1.
Course and Complications
With therapy, the prognosis for acne is good, if not excellent. The patient should understand that most therapies provide control of the disease rather than cure, and that improvement does not occur overnight. The only potential cure, other than time, for acne is isotretinoin. If improvement has not been noted after 2 months, more intensive therapy can be prescribed, including increased concentrations of the topical agents, increased dosage of the oral antibiotic, or change in the antibiotic therapy. Continued improvement in the disease is expected with continued therapy. Many patients can discontinue systemic antibiotics after 3 to 6 months, but most require prolonged (often lasting for years) maintenance therapy with topical agents. However, bacterial resistance to antibiotics is becoming more frequent, thereby limiting the usefulness of long-term antibiotic therapy for acne. If acne is not responding to systemic antibiotics and topical therapies, then referral to a dermatologist is warranted. Isotretinoin induces prolonged remissions, if not “cures,” in many patients.
Acne remits spontaneously with time, to a degree that varies widely. For individual patients, there is no way to predict in advance when they will “outgrow” their acne. The goal of therapy is to keep the condition under control as long as it is active.
The major complication of acne is its psychosocial ramifications, which can be devastating for some patients. Patients with severe cystic acne may even be socially ostracized. In an ironic quirk of timing, acne occurs at a time of life when personal appearance is a prime concern and self-consciousness is at its peak. Regardless of the severity of the acne, for patients seeking help (even those with apparently mild disease), the disease is important and deserves serious attention. Patients are not impressed with soothing advice that trivializes their disease and reassures them that they will eventually “outgrow” it.
In addition to the cosmetic liability of active lesions, scars further compound and perpetuate a poor self-image in some patients long after the acne has remitted. Scars are difficult to treat. Dermabrasion, laser “resurfacing,” chemical peels, and surgery have all been employed, with varying results. Because scars are more easily prevented than treated, the emphasis in acne is on early and aggressive medical therapy.
Pathogenesis
Multiple factors are involved in the pathogenesis of acne. The three most significant are:
Factors involved in acne pathogenesis:
- 1.
Androgens
- 2.
Follicular obstruction
- 3.
Propionibacterium acnes
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