Page 113 - The Netter Collection of Medical Illustrations - Integumentary System_ Volume 4 ( PDFDrive )

Plate 4-28 Rashes

DRUG ERUPTIONS
ERYTHEMA MULTIFORME,
STEVENS-JOHNSON SYNDROME,
AND TOXIC EPIDERMAL
NECROLYSIS (Continued)

in erythema multiforme major. Erythema multiforme
major is differentiated from erythema multiforme
minor in that it affects a larger surface area and affects
two mucous membranes.
In SJS, the dusky center of the lesion soon begins to
blister, first as small vesicles and then coalescing into
larger bullae. The extent and body surface area (BSA) Lichenoid drug eruption.
of blistering is used to differentiate SJS from toxic epi- Dusky purple macules and
dermal necrolysis. Most authors consider blistering of patches
10% of the BSA and involvement of at least two mucosal
surfaces to be definitive for SJS. Those cases with 10%
to 30% BSA involvement have been termed SJS–toxic
epidermal necrolysis overlap. Cases with greater than 30%
BSA involvement are considered to represent toxic epi-
dermal necrolysis. Light lateral pressure at the edge of
a bulla or vesicle is an objective physical test that can
be performed at the bedside. Spreading or an increase
in size of the blister with pressure indicates separation
of the epidermis from the underlying dermis and is
termed Nikolsky sign.
Pathogenesis: Erythema multiforme major/SJS is
believed to be a hypersensitivity reaction to certain
medications. The insulting medication is thought to be
metabolized into a recognizable antigen or to act as an
antigen without metabolic degradation. Antibodies
bind to the drug antigen and form antigen-antibody
complexes that can deposit in the skin and other
regions, causing an inflammatory cascade and the clini-
cal findings.
Histology: The classic histological picture of ery-
thema multiforme minor and major shows an acute
inflammatory infiltrate along the dermal-epidermal
junction. The stratum corneum is normal. There is an
interface dermatitis with vacuolar degeneration of the
basal cell layer. The interface dermatitis leads to necro-
sis and death of the basilar keratinocytes. If the necrosis
spreads and coalesces, small areas of subepidermal
blister formation may be seen. Erythema multiforme
minor can share some features with fixed drug erup-
tions. In fixed drug eruptions melanophages are typi-
cally present, whereas this is not the case in erythema
multiforme. Biopsy specimens of SJS and toxic epider-
mal necrolysis show more interface damage and blister- Erythema multiforme frequently
ing of the skin. The plane of separation is in the affects the palms.
subepidermal space.
Treatment: Therapy for erythema multiforme minor
and erythema multiforme major requires supportive
care. The skin lesions typically self-resolve with minimal
to no sequelae. Topical corticosteroids may help Resolving drug eruptions with secondary excoriations.
decrease the time to healing and decrease symptoms of Drug rashes typically start on the trunk and spread to
pruritus. Recurrent episodes of erythema multiforme the extremities.
due to herpesvirus infection can be treated with chronic
daily use of an antiviral agent such as acyclovir. This
decreases the recurrence of herpes simplex infection
and the resulting erythema multiforme reaction. Oral fluid and electrolyte balancing. Most patients with patients with infection-induced disease. If used late in
lesions can be treated with topical analgesics; the use of severe involvement will benefit from the experience of the course of disease, they appear not to help and only
oral steroids is reserved for severe cases. a burn unit. SJS and toxic epidermal necrolysis can be increase risk of side effects. Intravenous immunoglobu-
SJS can be a life-threatening condition and can prog- treated similarly to burns, because the same technical lin (IVIG) has been used to treat these conditions with
ress to toxic epidermal necrolysis. For both SJS and issues are involved. There is no consensus on how to varying success. If used early, it may modify the disease
toxic epidermal necrolysis, the cause of the reaction treat these two conditions with medications. The use of course; if used late, it is unlikely to be of any help. The
should be identified and withdrawn, and infections oral steroids early in the course of disease may help amount of BSA involved with blistering is related to the
should be treated appropriately. These patients require lessen the overall involvement, but steroids increase the prognosis. Those with greater BSA blistering tend to
aggressive supportive care, including wound care and risk of secondary infection and should not be used in fare worse than those with smaller BSA involvement.

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