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 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