Pediatric emergency medicine trisk 344

FIGURE 70.14 Inflammatory linear verrucous epidermal nevi (ILVEN). ILVEN is
notable for its often larger collections of verrucous plaques with background
inflammation.

Since lichen striatus resolves spontaneously in most typical cases, no
treatment is necessary. In those with symptomatic pruritus, topical steroids
may be considered for intermittent use.

VIRAL SYNDROMES
Viruses are involved as the presumed cause or trigger for a variety of
patterned skin disorders. Their specific identification is not always possible
in fully developed presentations, and this can be frustrating even for
seasoned clinicians. The difficulty in diagnosis is accentuated in the earliest
stages of the viral syndromes when the patterns may not yet be fully
established. Unfortunately, these patients tend to present much earlier in the
course of the disease to the emergency department than to dermatology.
Typically, these syndromes arise either during the acute phase of the disease
(as with Kaposi varicelliform eruption [KVE]), or as a reactive phenomenon
as the viral infection resolves (as with papular-purpuric gloves-and-socks
eruption [PPGS], unilateral laterothoracic exanthem [ULE], and Gianotti–
Crosti syndrome [GCS]).


FIGURE 70.15 Kaposi varicelliform eruption. Note the crusted vesicles and pustules
concentrated in areas where the pre-existing eczema has been active.

Kaposi Varicelliform Eruption
KVE is a collective term that indicates an acute, often rapidly progressive,
viral secondary infection of an underlying inflammatory skin condition (
Table 70.2 ). When herpes simplex virus, enterovirus, or vaccinia virus
secondarily infects the skin in atopic dermatitis, the condition is referred to

as eczema herpeticum (EH), eczema enteroviricum (coxsackium), or eczema
vaccinatum, respectively. Less commonly, inflammatory diseases such as
psoriasis, PRP, or blistering skin diseases like pemphigus vulgaris,
pemphigus foliaceus, keratosis follicularis (Darier disease), or benign
familial pemphigus (Hailey–Hailey disease) can become infected, usually
with herpes simplex virus and less commonly, varicella zoster virus.
Similarly, contact dermatitis, sunburn, or other more acute skin barrier
damage can provide a temporary opportunity for the same phenomenon to
occur outside of a chronic skin condition.
The hallmarks of the condition are the acute onset and rapid progression
of viral skin lesions. Initially localized vesicles or pustules will rapidly


spread and later evolve into monomorphic (all similar appearing) punchedout erosions ( Fig. 70.15 ). These cutaneous findings characteristically occur
at anatomic sites where the primary skin disease is either present or has
previously been located, and help to differentiate KVE from a primary (firstepisode) viral HSV or enteroviral outbreak.
TABLE 70.2
KAPOSI VARICELLIFORM ERUPTION
Phenomenon

Primary skin disease

Secondary infecting
virus

Eczema
herpeticum
Eczema
enteroviricum
(eczema

coxsackium)
Eczema
vaccinatum
Pityriasis rubra
pilaris
herpeticum
Keratosis
follicularis
herpeticum
Pemphigus
herpeticum

Atopic dermatitis

Herpes simplex virus

Atopic dermatitis

Enterovirus (coxsackie)

Atopic dermatitis

Vaccinia virus

Pityriasis rubra pilaris

Herpes simplex virus

Darier disease (keratosis
follicularis)

Herpes simplex virus

Pemphigus vulgaris,
benign familial
pemphigus (Hailey–
Hailey)
Psoriasis

Herpes simplex virus

Psoriasis
herpeticum

Varicella zoster virus

KVE may be accompanied by fever, mucocutaneous involvement,
malaise, and poor oral intake. Signs of bacterial superinfection (an infection


over an infection) with Staphylococcus aureus or Streptococcus pyogenes
may be present. S. pyogenes by itself may cause a secondary infection in an
atopic child that resembles eczema herpeticum, presenting with fever,
cellulitis, and clusters of pustular skin lesions.
The decision to admit to hospital should be determined by the degree of
toxicity. While patients may require in-hospital care for intravenous
hydration or intravenous antibiotic therapy to address widespread bacterial
infection or bacteremia, selected nontoxic patients with limited disease may
be successfully managed in the outpatient setting, as long as patients are
followed closely and reconsidered for admission if they do not respond

adequately or worsen clinically.
When a patient is suspected of having KVE, the initial history taking
should identify the existence of an underlying primary skin disease history,
its usual sites of anatomic involvement, and the suspected viral agent—
herpes simplex, enterovirus, vaccinia, or varicella zoster.
Recommended diagnostic studies include polymerase chain reaction
(PCR) assay, direct fluorescent antibody testing, or viral culture for herpes
simplex virus, varicella zoster virus, and if suspected, enteroviral PCR or
culture. Vaccinia virus may be considered in the appropriate exposure
context. Bacterial skin culture and blood culture for bacteria may be
obtained if a bacterial superinfection is suspected.
Recommended therapy involves empiric antiviral treatment with activity
against herpes simplex, such as acyclovir or valacyclovir. Empiric
antistaphylococcal and antistreptococcal coverage may be considered if
significant serous crusting is present, and especially if the child is febrile or
ill appearing. The optimal agent depends on local antibiotic resistance
patterns but will most likely include clindamycin, a first-generation
cephalosporin such as cephalexin or cefazolin, a penicillinase-resistant agent
such as oxacillin or nafcillin, or in more severe cases, vancomycin. If
trimethoprim-sulfamethoxazole is used, it may need to be combined with
another agent to provide adequate coverage for streptococci. Empiric
antiviral therapy for eczema herpeticum reduces the length of hospital stay
(LOS) when started promptly. As the antiviral medications are both
relatively safe and inexpensive, a low threshold for starting these agents is
recommended. In contrast, empiric systemic antibiotic therapy reduces LOS
only when there is bacteremia.