Adolescent Acne: A Stepwise Approach to Management

Iris Woodard, BSN, ANP

Disclosures

Topics in Advanced Practice Nursing eJournal. 2002;2(2) 

In This Article

Pathophysiology

Acne is a chronic disease involving the pilosebaceous follicles. Sebaceous glands are found most abundantly on the face and scalp, though they are present on every part of the skin except the palms of the hands and soles of the feet. Though the sebaceous gland is a mini organ, it is anatomically and functionally related to the hair follicle. Cutaneous disorders attributed to the sebaceous gland are really disorders of the entire pilosebaceous unit. The areas most commonly involved in acne are the face, upper chest, and back. Other less common areas include the upper arms, buttocks, and upper thighs.

Acne arises from the interaction of 4 factors[5]:

  1. Excess sebum production caused by androgenic stimulation of sebaceous glands;

  2. Outlet obstruction of the sebaceous follicle arising from excess production of keratinocytes (the basic cell of the epidermis);

  3. Increased proliferation of the bacteria Propionibacterium acnes that normally live in the sebaceous follicle; and

  4. Inflammation caused by sebum escaping into the surrounding skin.

Obstruction of the sebaceous follicle is the primary pathologic event in acne, giving rise to the micro-comedo, the precursor of all acne lesions. Once the follicle is plugged, its lower portion becomes engorged and distended with sebaceous discharge and keratinocytes. While the pore opening remains closed, the lesion is called a closed comedo, or "whitehead." The closed comedo is 1-3 mm in diameter, white or flesh-colored, and very slightly raised. Oxidization occurs when the follicle enlarges enough to stretch the pore and the trapped matter is exposed to air. This causes the characteristic dark appearance of open comedones or "blackheads." Open comedones are flat or slightly raised, brown-to-black papules about 3-5 mm in diameter.

Early acne, involving a majority of open and closed comedones, is a noninflammatory process. As dilation of the follicle continues, the follicular epithelium is disrupted and irritants such as sebum, hair, and keratinocytes are released into the surrounding dermis. This leakage causes an inflammatory reaction and initiates the formation of the inflammatory lesion papules, pustules, and nodules. Although P acnes is a live bacterium, living in the follicle, it dies when the follicular structure is disrupted. Toxins are released into the dermis, which increases inflammation. Therefore, uncomplicated, inflammatory acne is a sterile process and not a skin infection.[6]

As inflammation continues to worsen, larger papules and pustules are created. Acne papules are pink or red and 2-5 mm in diameter. Pustules contain grossly purulent material. Acne nodules are solid, raised inflammatory lesions that exceed 6-10 mm in diameter and are situated deeper in the dermis. The acne cyst is a large nodule that has suppurated and become fluctuant. Scars form as a result of damage to the surrounding dermis.[6] Scars may appear as small deep punched out pits ("ice pick"), atrophic macules, hypertrophic papules, or broad, sloping depressions.

In a person who is prone to acne, factors that may trigger or worsen the severity of the disease include:[5]

  • Pomade or gel used on the hair, which can cause acne on the forehead.

  • Prolonged use of topical or oral steroids, which can cause localized or generalized acne.

  • Certain oral medications such as lithium and phenytoin may worsen acne. Depo Provera injections for contraception may also worsen acne.

  • Friction from a tight strap on a sports helmet causes acne in the area being rubbed.

  • Excessive manipulation by the patient, causing the primary lesions to disappear and leaving excoriated, raw-looking marks. This is called acne excoriée and can cause scar formation.

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