Pediatric emergency medicine trisk 322

CHAPTER 67 ■ RASH: VESICULOBULLOUS
MARISSA J. PERMAN

INTRODUCTION
Basic to all vesiculobullous (blistering) disorders is the disruption of cellular
attachments. Blister formation, therefore, follows intracellular degeneration,
intercellular edema (spongiosis), or damage to the anchoring structures associated
with the basement membrane (hemidesmosomes, basal lamina, anchoring fibrils).
The location of these changes can help the physician ascertain a specific
diagnosis. When histologic information is not readily available or nondefinitive,
however, the historical and clinical features of the case must be relied on. This
chapter will discuss the following entities: infestations, mastocytosis, inherited
blistering disorders, acquired autoimmune bullous disorders, friction blisters, and
frostbite, as well as the differential and workup for these blistering skin disorders.

ACQUIRED BLISTERING ERUPTIONS
Infestations
Insect Bites
Insects generally bite exposed skin surfaces. Therefore, heaviest involvement
occurs on the head, face, and extremities. Mosquito bites occur in the warm
weather months, whereas flea (Pulex irritans ) bites and bed bug (Cimex
lectularius ) bites occur throughout the year. Historical information should
address contact with pets, recent camping trips or involvement in outdoor
activities, and known exposure in close contacts. When blisters are present, the
more characteristic urticarial papules are usually present in nearby locations,
often clustered together or aligned linearly. This linear arrangement is often
referred to as “breakfast, lunch, and dinner.” The differential includes bullous
impetigo, which can easily be ruled out with a Gram stain or bacterial culture. In
the case of bullous insect bites, the lesions should be negative for bacteria but can
occasionally become secondarily infected.
If there is concern for flea bites, all pets should be evaluated by a professional.

Bed bugs can be very difficult to locate but may be detected by turning on the
lights late at night and inspecting along the mattress seams and legs of the bed.
Symptomatic treatment for insect bites includes mild to moderate potency topical
corticosteroids and antihistamines such as diphenhydramine.


Scabies
While scabies in older children and adults most commonly presents as numerous
ill-defined scaling, erythematous papules, interdigital scaling, and lesions in folds
such as the umbilicus, groin, and axillae, infants and very young children can
have vesiculobullous lesions on the palms ( Fig. 67.1 ), soles, head, and face. It is
important not to be misled by this distribution and appearance. Occasionally, the
lesions can be nodular and often involve the genitals and axillae in young
children. Generally, the parents or other close family contact are also affected and
exhibit the typical appearance and pruritus of this disorder. First-line therapy for
scabies includes permethrin cream (from the head down in infants age >2 months
and older, neck down in older children and adults) applied twice, 1 week apart,
and washing all fomites in hot water followed by drying on high heat. Fomites
not amenable to washing may be dry-cleaned or placed in an airtight bag for
several days. All close contacts should be treated. Ivermectin has also been used
successfully.

Acropustulosis of Infancy
The appearance of pruritic vesicopustules in infants and young children on the
palms and soles ( Fig. 67.2 ) may also suggest acropustulosis of infancy. Vesicles
often involve the lateral aspects of the fingers, palms, and soles. This condition
may be misdiagnosed as dyshidrotic eczema and is similarly pruritic. Some
speculate a relationship with antecedent scabies infestation in a subset of patients
and may refer to this phenomenon as postscabetic pustulosis in this setting.
Cyclic eruptions occur every 2 to 3 weeks, lasting 7 to 10 days. Spontaneous

disappearance occurs at 2 to 3 years of age. Treatment with topical steroids may
moderate some of the pruritus.
For a complete differential of acute vesiculobullous eruptions involving the
palms and soles, see Table 67.1 .

MASTOCYTOSIS
Cutaneous mast cell disease (mastocytosis or urticaria pigmentosa) may cause
blistering in young children and may be associated with activating c-KIT
mutations. Red-brown lesions ( Fig 67.3A ) that blister after stroking or trauma
(Darier sign) indicate the release of histamine from mast cells ( Fig 67.3B ). This
collection may be isolated (mastocytoma) or generalized (urticaria pigmentosa or
bullous mastocytosis). In addition to stroking, other triggers include mast cell
destabilizers such as nonsteroidal anti-inflammatory drugs (NSAIDs), polymyxin
B, some anesthetic medications (both topical and systemic), venom from bees or
wasps, and narcotics. Additionally, extreme temperatures or sudden changes in


temperature may lead to mast cell destabilization and histamine release. Refer to
www.mastokids.org for more information about common mast cell degranulation
triggers. Blistering of such lesions generally occurs in the first few years of life.
After this time, urticaria occurs more often than blistering. Lesions may be
generalized and are often associated with more severe cutaneous disease or rarely
systemic mastocytosis. When a presumed melanocytic lesion feels infiltrated, the
physician should think of mastocytosis—Darier sign will confirm the diagnosis.
If asymptomatic and localized, active nonintervention is appropriate. For
symptomatic disease, primary treatment is aimed at preventing histamine release
with H1 and H2 antihistamines. The majority of patients have regression over
time.

FIGURE 67.1 Blisters on hands of a child with scabies.

FIGURE 67.2 Note vesicles and pustules on a child’s palm with acropustulosis of infancy.