SAMATHA MADHAVARAPU

PGY-1

6 m/o with rash on face

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

Other diseases assoc with KVE Mycosis fungoides Pityriasis rubra

pilaris Neurodermatitis Irritant contact

dermatitis Congenital

ecthyosiform erythroderma

Ichtyosis vulgaris Rosacea

Benign familial pemphigus

Wiscott Aldrich Syndrome

Sezary syndrome Seborrheic

dermatitis Skin grafts/Burns Cow pox Cutaneous T cell

lymphomas

DD

Chicken pox Contact dermatitis, allergic Impetigo VZ virus Eczema vaccinatum

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.