EPIDERMAL INCLUSION CYST
Epidermal inclusion cysts are the
most common benign cysts derived from the skin. They are also known as
epidermoid cysts or follicular infundibular cysts. The name “sebaceous cyst”
has been used to describe these cysts, although this is a misnomer, because
epidermal inclusion cysts are not derived from sebaceous epithelium. The cysts
can occur anywhere on the body except the palms, soles, glans, and vermilion
border.
Clinical Findings: Most epidermal inclusion cysts are
subcutaneous nodules that vary in size from 5 mm to more than 5 cm. They have
no race predilection but are seen more commonly in men than in women. Onset
most commonly occurs during the third decade of life. The nodules
characteristically have an overlying central punctum. From this punctum,
drainage of white, cheese-like material, which represents a buildup of
macerated keratin debris, can occur. Most small epidermal inclusion cysts are
asymptomatic, and they rarely cause a problem.
Larger epidermal inclusion cysts can become irritated and inflamed. If
the inflammation is severe enough, the cyst wall ruptures. When the cyst
contents enter the dermis, the keratin sets off a massive inflammatory reaction,
which manifests clinically as edema, redness, and pain. Once this has occurred,
patients often seek medical advice.
The main differential diagnosis for a ruptured epidermal inclusion cyst
is a boil or furuncle. Ruptured epidermal inclusion cysts are almost never
infected, although infection can occur within a longstanding ruptured cyst that
has not been treated. The main differential diagnosis of an unruptured,
noninflamed epidermal inclusion cyst is a pilar cyst. Pilar cysts do not have
an overlying central punctum, and this is the easiest means of differentiating
the two cyst types. Pilar cysts are also more common on the scalp. Milia are
considered to be tiny epidermal inclusion cysts.
Histology: The epidermal inclusion cyst is a true cyst with
an epithelial lining of stratified squamous epithelium and an associated
granular cell layer. The central cavity is filled with keratin debris. The cyst
is derived from follicular epithelium.
Pathogenesis: The epidermal inclusion cyst is derived from
the infundibulum of the hair follicle. Epidermal inclusion cysts occur as the
result of direct implantation of epidermis into the underlying dermis; from
there, the epidermal component continues to grow into the cyst lining. Many
researchers have looked at the roles of ultraviolet light and human
papillomavirus infection in the etiology, but no definitive conclusions on
either have been drawn.
Treatment: Small cysts that are asymptomatic do not need to
be treated. One should advise patients not to manipulate or squeeze the cysts.
Such trauma could cause rupture of the cyst wall and set off an inflammatory
reaction. Small cysts can be cured by a complete elliptical excision, making
sure to remove the entire cyst wall.
If a small portion of the cyst wall is left behind, the cyst is likely to
recur.
Inflamed cysts should be treated initially with an incision and drainage
technique. The region is anesthetized and then incised with a no. 11 blade. The
resulting cheesy-white macerated keratin debris is removed with lateral
pressure, and a curette is used to break apart internal loculations. The
drainage material has a pungent odor.
The resulting cyst cavity can be packed or left open until the patient returns
in 2 to 3 weeks for definitive removal of the cyst lining by excision.
Intralesional triamcinolone is very effective in decreasing the inflammation
and pain in these inflamed cysts. Long-standing cysts should be cultured and
the patient given the appropriate antibiotic therapy based on the culture results.
