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SAMATHA MADHAVARAPU PGY-1. 6 m/o with rash on face.

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Presentation on theme: "SAMATHA MADHAVARAPU PGY-1. 6 m/o with rash on face."— Presentation transcript:


2 6 m/o with rash on face

3 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

4 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

5 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

6 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

7 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/.

8 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.

9 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

10 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

11  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

12  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.

13 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.

14  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.

15  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

16 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

17 DD  Chicken pox  Contact dermatitis, allergic  Impetigo  VZ virus  Eczema vaccinatum

18 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.

19  Consult Ophthal: If eye involvement is suspect  Herpetic keratitis can cause scarring  Ocular herpetic infection in setting of KVE is rare.

20 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

21  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

22 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.

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