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RASHES IN THE PEDIATRIC ER: WHEN TO WORRY?
Molly W. Stevens, MD, MSCE
INFECTION: BACTERIAL
Bacterial toxin-induced: Scarlet fever, SSSS, TSS are caused by circulating toxins rather than direct invasion
Scarlet Fever: exanthum caused by toxin released from strep (sometimes staph)
-most frequently seen in children 2-10 yrs old
-erythematous fine macules and papules (sandpaper rash), first on neck and face, spreads down over
trunk, extremities; may at times be petechial; spares palms and soles; often generalized
adenopathy
-strawberry tongue with strep but not staph scarlet fever (initially white, then red)
-staph scarlet fever characterized by impressive skin tenderness and crusting around nose, mouth,
eyes but not bullous mucous membrane involvement
-superficial desquamation as rash fades (hands, feet, inguinal)
-treat with penicillin, erythromycin, dicloxacillin
-rare complications: bacteremia, rheumatic fever, pneumonia, meningitis
Toxic shock: staph (MTSS or non-menstrual) or strep (skin infection with toxin production: cellulitis,
necrotizing fasciitis, puerperal sepsis, rarely strep pharyngitis)
-both seen in kids, strep more common in younger; high mortality 25-50%
-rapid onset fever/ hypotension/ tachycardia, tachypnea
-early: diffuse erythroderma and mucosal erythema (looks like early scarlet fever), see mild edema
facial, hands, feet, “painless sunburn”, strawberry tongue, to full scarletineform rash, bulbar
conjunctival injection and/or subconjunctival hemorrhage, mucous membrane ulcers
-organ hypoperfusion and multi-system failure, acral necrosis
-late: desquamation in early convalescence
- aggressive support; treat infection (stop toxin production, clindamycin to block protein synthesis)
Impetigo: superficial involvement (only to mid-epidermis); streptococci, staphylococci or both
-begins as erythematous macules, progresses to small thin-roofed vesicles or bullae with mild erythema
and serous discharge, to classic ‘honey-crusted’ lesions; larger flaccid bullae in staph
-minimal tenderness
-exudate will spread lesion (autoinoculation) causing characteristic satellite lesions
-staph: often causes bullous impetigo; like a localized “scalded skin”; local release of
epidermolytic toxins; intertrigo
-strep: vesicular-pustular lesions, can look like small ulcers
-treat topically for mild cases; systemic for young, more severe or generalized
Ecthyma: deep or ulcerative type of pyoderma; full-thickness dermal involvement, small and punched out, or spreading ulcer
-begins like impetigo, but penetrates fully thru epidermis (deeper lesion than impetigo when crust removed; very tender, can
have a halo of cellulitis; often heals with scarring
-treat with systemic antibiotics
Staph scalded skin: dermatosis caused by bloodstream dissemination of epidermolytic toxins A&B
produced by certain staph (phage grp II coag.+staph; target cell-cell adhesion [desmoglein]; stratum
corneum and granulosum)
-infants, young children, and immunosuppressed or renal patients
-begins like staph scarlet fever with malaise, fever, irritability, and generalized macular erythema,
progresses to extremely tender scarletineform rash; then to exfoliative phase beginning with
exudates/crusting around mouth/eyes/nose, upper layer of epidermis “peeling off like wet tissue
paper” to minor trauma (Nikolsky sign), then to desquamation phase with large flaccid bullae
and later exfoliation of skin, heals without scarring (if no superinfection)
-complications: secondary infection, fluid/electrolyte loss
-treat with systemic antibiotics
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Cellulitis: acute suppurative inflammation mainly of loose subQ CT, may go deeper
- spread from wound, hematogenous, or deeper infection
-charac. by tenderness, erythema, swelling, warmth; borders not elevated or sharply defined
-grp A B-hemolytic strep/ staph. A/ H. flu/ Strep pneumo
-specific sites as special cases: orbital, periorbital, buccal
-erysipelas: superficial cellulitis, marked lymphatic involvement; raised advancing edges, sharp borders, (“orange peel”)
Necrotizing fasciitis: rapidly progressive, often fatal, infection of deep fascia with extensive subQ necrosis
-hemolytic strep (most often in kids), GABH strep, staph a., proteus, bacteroides, hemophilis, or
other mixed aerobic/anaerobic flora; 50% myonecrosis, ~25% progress: toxic shock, organ failure
-acute or with chronic dz; incr risk after trauma/surgery, IDDM, immunosuppression, NSAIDS
-progresses rapidly from cellulitis with fever to have central blue discoloration, ulceration, gangrene,
and systemic toxicity/ from cellulitis to fasciitis and myonecrosis/pyomyositis (GU is Fourniers
gangrene); 35% with crepitus; lab findings include elevated WBC, Na<135; BUN>15.
-suspect with unusually tender and indurated cellulitis; ill-appearing beyond expected
- severe pain, induration, bullae, cyanosis, skin pallor, weakness, hypesthesia then numb
-signs of sepsis (TSS) with incr. HR and RR; oliguria, confusion, high CK /CRP, bandemia,
-prompt surgical debridement/ IV antibiotics/ supportive care; 20-30% mortality, +sepsis mortality 70%
NOT Cellulitis: if it’s warm and red, but not tender and not ill, very likely NOT bacterial infection
Examples: rhus dermatitis, insect bites or bee stings; contact dermatitis; atopic dermatitis, dental
infection reactive erythema, popsicle panniculitis
INFECTION: HUMAN HERPES VIRUS
VARICELLA ZOSTER VIRUS: cases to worry about
Neonatal varicella: just after birth; no benefit from maternal ab via placenta; at risk for severe
disseminated infection, pulmonary and hepatic involvement, hemorrhagic lesions to purpura fulminans;
high mortality if not treated early
Purpura fulminans: rare in healthy children; presentation of varicella in immunocompromised children
HERPES SIMPLEX: cases to worry about
Keratitis (primary or recurrent infection):
-has potential for scarring/ loss of visual acuity;
-small punctate or dendritiform ulcerations may be seen on fluorescein exam
-ophthalmology consult for any suspected HSV corneal lesion, or if periorbital/facial lesions with
conjunctival injection/ eye pain/ epiphoria even if no grossly fluorescein + lesions appreciated
Eczema herpeticum (Kaposi’s varicelliform eruption)
-generalized HSV infection in children with atopic dermatitis, burns, or other conditions with
disruption of epidermal barrier
-characterized by high fever, malaise, can have hundreds of skin vesicles (punched-out
appearing erosions); treat like a burn patient when extensive
Neonatal HSV:
-approx. 10% of infants born to parent with active infection; 2/3 HHV-2; 1/3 HHV-1
-rash may appear anytime first week or more after birth; classic herpetic or atypical, subtle/extensive
-cutaneous, systemic, and neuro-cutaneous forms
-may be confused with the other TORCH congenital infections (toxoplasmosis, other viruses and cong.
syphilis, rubella, CMV, and HSV), neonatal bacterial sepsis
-high occurrence disseminated dz
*consider treatment for HSV for any sick neonate (first two weeks of life) pending culture
results; examine sick neonates carefully for vesicular or crusted rashes
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PETECHIA / PURPURA:
HSP: Most common vasculitis in children; immunologically mediated (IgA vasculitis), non-thrombocytopenic
systemic vasculitis (skin, GI tract), jts; with renal involvement: look for hematuria, cellular casts, proteinuria,
htn, elevated BUN or Cr
-treat with steroids only if painful arthritis or abd pain, renal involvement; aggressive tx of htn if renal
involvement; frequent urine checks for 6 months even in mild cases.
ITP: now called autoimmune thrombocytopenic purpura; isolated thrombocytopenia (plt autoantibodies); abs
generated in response to foreign antigen or drug cross-rxn with plt membrane glycoproteins; usually selflimited; win-rho ((anti-Rh-D immunoglobulin), IVIG, steroids, or just careful observation without tx
RMSF: most common rickettsial dz in US; mortality 5-10%; southern Atlantic, south central states most
frequent (AK, LA, OK, TX, KT, TN, AL, MI)
-90% cases Apr-Sept, wooded and high grass areas, American Indians, whites, males, and children
-transmitted by Rickettsia rickettsia (gr-); hosts: wood tick in the west, dog tick in the east; causes
multi-organ vasculitis (skin/adrenals most common), vascular permeability: edema,
hypoalbuminemia, hyponatremia, thrombocytopenia, and hypotension; cardiac/renal failure, meningitis,
pneumonitis.
-clinical dx: fever, HA, rash (n/v, myalgias, anorexia, abd pain); rash occurs in 80-90% pts 2-5 days
after fever starts; maculopapular to petechial, then w/ ecchymoses; wrists/ankles, to soles/palms, then
extremities to trunk; spares face (40% palms and soles only).
-doxycycline; tetracycline, chloramphenicol; increased mortality for delayed abx after 5th day, or
G6PD
Meningococcemia: Neisseria meningitides; thirteen serotypes; B,C, and Y most US cases
-colonization to dissemination to fulminant dz
-Fulminant dz signified by diffuse micro vascular damage; DIC, septic shock, death from endotoxic
shock with circulatory collapse and myocardial dysfunction; death in greater than 20% of
fulminant course (lower in meningitis at 5%)
-Rash: nonspecific maculopapular to morbilliform or urticarial, with rapid progression petech/purpura
-poor prognosis: no meningitis, shock, coma, purpura, neutropenia, thrombocytopenia, DIC,
myocarditis
-treat petechial rash and fever with abx; aggressive management any signs systemically ill
ALLERGIC/ HYPERSENSITIVITY:
Urticaria (hives):
-release of vasoactive substances (histamine and other cytokines) with plasma extravasation into local
tissue, then resorbed (lesions transient)
-classified as immune and non-immune mediated:
-immune mediated: type I, II, III allergic
-non-immune mediated: complement (viral, bacterial inf/serum sickness/transfusion rxn), or
physical stimuli
-hypersensitivity response to infection, insect stings/bites, medications, foods, or inflammatory
systemic disease (such as SLE, JRA, CVD, IBD, Crohn’s, UC)
-sudden onset, pruritic (mild or severe), erythematous, raised wheals (flat-topped, edematous, firm,
warm); edema in superficial dermis= hives; in deep derm or subQ= angioedema
-often mistaken for EM, but individual lesions are transient, usually lasting 20 min to 3 hours, reappear
in other areas; episodes usually 24-48 hours, but can last 3 weeks (chronic urticaria >6wks)
-lesions can be giant (30 cm); can be accompanied by subQ extension (angioedema of face/neck,
hands/feet, overlying joints, or GU most common in children)
-treat with antihistamines; no evidence to support use of systemic steroids; ?doxypin
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EM (Erythema Multiforme):
-“Hypersensitivity Syndromes” include EM, SJS, TEN, erythema nodosum
-type IV hypersensitivity
-deposition of IgM in superficial microvasculature
-acute onset of oval/round, fixed (same site at least 7 days), erythematous lesions that progress to
concentric zones of color change: central is dusky, blistered or crusted (area of epidermal
injury can be cyanotic, purpuric, or vesicular).
-no prodromal symptoms
-lesions begin dorsum hands/ extremities; often palms and soles; mild mucosal involvement
-most cases thought to be due to HSV specific host response to HSV antigens in keratinocytes; may
also be due to mycoplasmal antigens, EBV, CMV, other human herpes viruses; perhaps
other hypersensitivities to viral, bacterial, protozoal, fungal, or, or food/drug sensitivity
-usually lasts approx. 3 weeks; can recur
-acute urticaria often confused with early EM (but lesions not fixed >24 hours!)
-treat with symptomatic relief (compresses, antihistamines); consider trial of acyclovir/gancyclovir in
recurrent episodes; +/- treatment with steroids (may increase risk of recurrence if due to HSV),
recurrence may be induced by sun exposure, stress; recurrent lesions
acyclovir/dapsone/antimalarials/azathioprine
Stevens-Johnson Syndrome/TEN:
-life-threatening/mucocutaneous hypersensitivity syndrome/ extensive necrolysis and
detachment of epithelium (deposition of immune-mediated complexes; apoptosis of
keratinocytes; cell-mediated cytotoxic rxn; histopathology is full-thickness necrosis);
5% mortality SJS, 30% TEN
-initial cutaneous lesions similar to EM, but early central blisters move to severe epidermal
necrosis/ loss of epidermis within hours; large bullae may cause loss of sheets of epidermis
or mucosa; SJS: the mouth is always affected, severe mucous membrane involvement;
begin face/trunk and spreads; palms/soles erythematous and painful
-distinct prodrome (flu-like) lasting 1 to 5 days of fever, myalgias, headache, ST, malaise, arthralgia,
pharyngitis (+/-cough, vomiting, diarrhea)
-mild to mod skin tenderness/pain, paresthesias, anxiety, photophobia, keratitis, corneal erosions;
+/- RTN, ARF, hypotension, respiratory failure, sz, coma
-SJS mucosal involvement/ erosions/necrosis; involves at least two mucosal surfaces
-TEN (toxic epidermal necrolysis) has similar cutaneous findings, may occur without mucosal
involvement; TEN with > 30% body surface area with epidermal detachment (SJS <10%)
-most cases drug induced (most commonly NSAIDS, sulfonamides/abx, anticonvulsants,
antihypertensives, and allopurinol); etiology also includes malignancies, viral (HSV, EBV, entero-,
influenza), and bacterial (mycoplasma, GABH strep) infections, radiation, pregnancy, CTdz
-treat as burn patient; discontinue offending drug; ophtho consult; consider IVIG; aggressive fluid and
electrolyte replacement, nutritional support, and infection prophylaxis; steroids very
controversial (early and short if at all); IVIG; TEN treatments incl cyclosporine, plasmapheresis
References:
Block, SL. The Many Faces of Facial Cellulitis. Pediatric Annals, May 2013. 42(5):187-190.
Cherry JD, Harrison GJ, Kaplan SL, Steinbach WJ, and Hotez PJ. Feigin and Cherry's Textbook of Pediatric Infectious Diseases, 7th Edition. Saunders, 2014. Chapter
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Dermatology Image Atlas, Dermatlas.org (http://dermatlas.med.jhmi.edu/derm/). Accessed 2/2011 and 11/2009.
Fustes-Morales A, Gutierrez-Castrellon P, Duran-Mckinster C, et al. Necrotizing Fasciitis Report of 39 Pediatric Cases. Arch Dermatol. 2002;138(7):893-899.
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