HPI Worsening rash on the face since 3 days Rash initially on R cheek Spread to R eyelids and L side of face x 1 day Baby has been scratching it Rash was associated with some blisters assoc with oozing, bleeding and scabbing H/o fever + Tm 102 F
HPI Contd Crying a lot No URI symptoms/ GI symptoms Good P.O Normal urine output Sibling has similar rash around her mouth No daycare No recent travel No pets
PMH : h/o eczema + uses aquaphor No surgeries, no hospitalizations BHx: FTNSVD, Birth wt: 5lbs 8 oz. Pregnancy was uneventful Imm: UTD All: NKDA DHx : Enfamil 6 oz every 3-4 hrs Devpt: Appropriate for age FHx : no eczema, no asthma. SHx : lives with mother, grandmother and 2y/o and 3y/o siblings
Physical Examination VS: 98.9 F, HR: 132, RR: 32, PO2 99% HEENT: AFOF, PERRLA, conjunctival erythema+ swollen R eyelidsOP: MMM, b/l TM n Post occipital nodes + RRR, S1+, S2+ no murmur Lungs: CTA b/l Abd: soft, NT, ND, BS+ Ext: FROM x4, cap refill < 2 sec, pulses +2
Physical Examination Skin: Impetiginous lesions, some scabbing, some vesicular and wet lesions over R cheek, R upper and lower eyelids, L upper eyelid. Labs: CBC : 11.4, 17/ 36.8/ 347/ N: 33.9/L: 53.4 3.9/ 64/ 2.5/ 39/.
ECZEMA HERPETICUM Kaposi varicelliform eruption Refers to herpetic superinfection of pre- existing skin disease. HSV 1, HSV 2, Coxsackie A 16, Vaccinia In preexisting dermatoses Most common: Disseminated HSV infection in pt with Atopic Dermatitis.
Pathophysiology Disruption of stratum corneum sec to skin disease is most common predisposing factor. Involves both cell mediated and humoral defects in persons with atopic dermatitis. T cell mediated immunity to control primary and recurrent HSV Antibodies against HSV limit the severity of infection Reduced NK cell number and IL-2 receptors, a marker for lymphocyte activation
Pathophysiology One study- skin in pts with AD is rich in IL- 4 which inhibits Th-1 cells and supress INF –gamma secretion Cathelicidin is antimicrobial peptide, component of innate immune response. Low levels of cathelicidin protein expression seen in eczema herpeticum pts Inverse correlation between cathelicidin expression and serum Ig E levels in KVE
High levels of IgE increase the risk for EH Corticosteroid Rx increases risk. Retrospective analysis of 100 cases of KVE -> 75% did not get it in 4 weeks before onset. Some showed showed topical clacinuerin inhibitors, tacrolimus increased risk. Immunosuppression Increased incidence of KVE since 1980, due to increased HSV infections Mortatilty from KVE decreased from 50% to <10% due to IV Rx
Effects men and women equally Thought to be disorder of infants, can effect children of any age. German study : 75 patients, age of onset 5 months to 69 yrs Mean age of onset of AD was lower (5.6 yr) in pts with KVE compared with AD controls.
History Begins as clusters of umbilicated vesiculopustules in areas of preexistent dermatitis. They progress to punched out erosions, pathognomonic of KVE Usually prediliction for upper body and head. Vesicles become hemorrhagic and crusted Erosions coalesce to large denuded areas, bleed and secondarily infected.
Often diagnosis is delayed Eruption continues to spread over 7 -10 days and assoc with high temperature, malaise, and lymphadenopathy. Primary episode of KVE runs its course and heals in 2-6 weeks.
Average duration of illness is 16 days Transmitted by contact with an infected person or by dissemination of primary or recurrent herpes Recurrent episodes may also occur, but milder and not assoc with systemic symptoms Some studies showed a high frequency of HSV DNA in the oral cavity of pts with KVE In severe cases, lesions heal with scarring
Labs Viral Cultures of fresh vesicular fluid and DFA stain –most useful and reliable Swabbing should be done vigorously as HSV is cell assoc and paucity of extracellular virus particles may be present DFA staining as accurate as viral cx. Available in hrs. Tzank smear: epithelial multinucleated giant cells and acantholysis If lesions are atypical, equivocal, or old, consider PCR or biopsy.
Consult Ophthal: If eye involvement is suspect Herpetic keratitis can cause scarring Ocular herpetic infection in setting of KVE is rare.
Treatment Nucleside analogs: Acyclovir Acts by inhibiting viral DNA polymerase Systemic / Topical antibiotics for secondary bacterial infections Dose: 15mg/kg/d IV tid for 5 days or until lesions heal
Foscarnet: For immunocompromised host with HSV and acyclovir resistant HSV Poor clinical response / persistant viral excretion indicates viral resistance Vidarabine, Trifluridine, Valacyclovir F/U care in 2 weeks to evaluate response to treatment
Complications Systemic Viremia: Liver, lungs, brain, GIT adrenal glands Septicemia from secondary bacterial infections of skin Staph aureus, group A beta hemolytic strep, Pseudomonas and Peptostreptococcus Ocular involvment: blepharitis, conjunctivitis, Keratitis, uveitis. Blindness due to stromal scarring. Very few ocular herpetic disease in KVE, even with + conjunctival HSV cx.