(+)Heather M.

Murphy-Lavoie, MD
Assistant Residency Director and
Assistant Professor, Louisiana State
University, Section of Emergency
Medicine, New Orleans, Louisiana
Recognizing the Top Ten
Pediatric and Adult Rashes

What is it, and what can I do about it? This is
what emergency physicians really want to know
when faced with a patient who has a rash. The
speaker will describe how to recognize ten
common and clinically significant rashes as
well as look-alike rashes. The appropriate
management and disposition of each rash will
be discussed. In addition, pearls for
distinguishing look-alike rashes will be
presented.

Describe the most common clinically
significant pediatric and adult rashes.
Identify these rashes by their presentation.
Differentiate among clinically significant rashes
that have similar presentations.


SU-153
10/16/2011
4:00 PM - 4:50 PM
Moscone Convention Center


(+)No significant financial relationships to disclose

Recognizing the Top Ten Pediatric and Adult Rashes
Heather Murphy-Lavoie, MD
OBJECTIVES
Describe the most common clinically significant pediatric and adult
rashes
Identify the rashes by their presentations
Differentiate among clinically significant rashes that have similar
presentations
Understand the pathophysiology and treatment of dangerous disease
states which present with rash

MACULOPAPULAR RASHES
1. Classic Exanthems and other viral rashes
Historically, six infectious exanthems were described: measles (rubeola), scarlet fever,
rubella, Dukes (4
th
disease), erythema infectiosum (fifths disease), and roseola. The majority of
childhood exanthems are nonspecific and cannot be accurately assigned to a discrete etiologic
diagnosis. These exanthems are typically self-limiting and resolve spontaneously within a week.
Measles
Measles is rarely seen in developed countries due to widespread use of the MMR
vaccine. However, measles continues to be problematic in developing countries. In 1997 it
remained the 6
th
leading cause of death worldwide, and it is still a leading cause of blindness in
children in Africa. The causative agent is paramyxovirus. Measles has an incubation period of 7
- 12 days and occurs most commonly in winter and spring. Its contagious 3 days prior to, and up
to 5 days following, the onset of the rash. Presenting signs and symptoms include a prodrome of
gradually increasing high fever (often >104 degrees Fahrenheit), coryza, dry hacking cough,
headache, and an impressive bilateral conjunctivitis. This prodrome occurs 2 - 4 days prior to
the appearance of the rash. Kopliks spots may appear on the buccal mucosa opposite the 2
nd

molars during this time. While not always seen, Kopliks spots are pathognomonic of measles.
After approximately 3 days, an erythematous, nonpruritic, maculopapular rash appears, first
behind the ears and at the hairline, and then spreads inferiorly. As the rash spreads to involve the
trunk and extremities, the discrete macules coalesce. After approximately one week, the rash
fades. Diagnosis is typically clinical, however, laboratory diagnosis can be accomplished by
serologic assays if necessary. Treatment of measles is primarily supportive. Administration of
vitamin A is associated with a reduction in the risk of mortality and a reduction in the post-
measles pneumonia complications in children less than two years old. (Yang 2005) Potential
complications include blindness secondary to corneal ulcerations, pneumonia,
laryngotracheobronchitis, otitis media, myocarditis and encephalitis. Mortality ranges from 0.3%
in developed countries to 26% in undeveloped countries.

Scarlet fever
Scarlet fever is a toxin-mediated condition characterized by fever, oral mucosa
involvement, and a rash. It usually occurs in children <ten years old. Scarlet fever is most often
associated with streptococcal tonsillopharyngitis, although it can be seen after other streptococcal
infections. The incidence is highest late fall to late winter.

Scarlet fever has an incubation period
of 2 - 5 days prior to the appearance of the rash. Presenting symptoms include: abrupt onset of
fever, headache, malaise, odynophagia, and occasional vomiting and abdominal pain. These
findings are followed by an enanthem consisting of bright red oral mucosa, palatal petechiae
(Forschheimer spots - punctuate erythematous macules on the palate and uvula), and a
strawberry tongue. A rash follows the onset of fever by 1 - 2 days and has been described as
generalized erythroderma with scattered pinpoint, erythematous blanching papules, giving the
rash a sandpaper-like texture. Capillary fragility causes petechiae in the flexural surfaces
(Pastias lines), and facial flushing with circumoral pallor is often apparent. The palms and soles
are typically spared. The exanthem typically resolves in 5 days, followed by post-exanthematous
desquamation, especially on the palms and soles, after about 2 weeks. Diagnosis is typically
clinical, but can be confirmed by streptococcus-positive culture of local infection such as
pharynx. Penicillin remains the treatment of choice of streptococcal pharyngitis in order to
prevent local suppurative complications and acute rheumatic fever. Complications are rare, but
include: acute rheumatic fever, acute glomerulonephritis, sepsis, pneumonia, pericarditis,
hepatitis, otitis media, meningitis, and toxic shock syndrome.

Untreated the mortality for scarlet
fever is 15-20% but is reduced to <1% with appropriate antibiotics.
Rubella
Rubella is a relatively mild illness caused by the rubivirus, and is characterized by a
maculopapular rash. Rubella has an incubation period of 12 - 23 days, with a period of
infectivity, which extends from a few days before until 7 days after rash onset. Rubella occurs
most commonly in later winter and early spring.

The prodrome, if present, is mild and consists
of malaise, pharyngitis, cough, low-grade fever, coryza, and a headache. A faint pink/red
maculopapular rash then appears, first on the face, then rapidly spreading inferiorly. The rash
typically resolves in 3 - 4 days. While the prodrome commonly occurs in adults and adolescents
1 - 5 days prior to rash onset , it is often absent in younger children. Other clinical findings
include: posterior cervical and occipital lymphadenopathy, Forchheimers spots, arthralgias, and
neutropenia. Diagnosis is clinical, however, serologic tests can be used for confirmation as
needed. Treatment for rubella is supportive and patients should be counseled to avoid pregnant
women. Potential complications of rubella include arthritis, encephalitis, thrombocytopenia, and
congenital rubella syndrome when maternal exposure occurs in the first trimester. Mortality is
less than one in 10000 for typical pediatric cases; however, cases of the congenital rubella
syndrome can cause birth defects including: hearing loss, congenital heart disease, mental
retardation, visual deficits, and numerous other neurologic and endocrine disorders including the
blue berry muffin syndrome.
Erythema infectiosum
Erythema infectiosum, otherwise known as fifth disease, is caused by human parvovirus
B19, and typically affects school-aged children. It has an incubation period of 1 - 2 weeks and
occurs more frequently in winter and spring. Children with this virus typically feel well,
however, about 10% of patients experience a prodrome consisting of low-grade fever, headache,
sore throat, malaise, myalgias, and coryza.

This prodrome is followed by a bright, fiery, red
macular rash across the cheeks, giving the child a slapped cheek or sunburned appearance.
This rash lasts 1 - 4 days, and progresses into a more generalized, lacy and reticular pattern, most
prominent on the extensor surfaces of the extremities. The rash may then wax and wane over the
following month, increasing in intensity with various stimuli.

Once the rash appears, these
children are no longer infectious.

Diagnosis is clinical, but serologic tests are available for
confirmation if necessary. Treatment of erythema infectiosum is usually supportive, but is
important to advise parents to keep the ill children away from pregnant women and those with
hemolytic anemias. High-risk groups may be treated with intravenous immune globulins.
Complications are rare but include symmetric arthritis of the hands, wrists, or knees, and
intrauterine infection and fetal death if the infection occurs during the first half of pregnancy.
Patients with hemolytic anemias and hemoglobinopathies (particularly sickle cell disease) are
prone to transient aplastic crisis when infected with parvovirus.
Roseola
Roseola is the most common viral exanthem in children <3 years. . The causative
agents of roseola are human herpes virus 6 and 7.

Roseola has an incubation period of 5 - 15
days. It is characterized by a high fever of 2 - 5 days duration in an otherwise well-appearing
child, followed by resolution of the fever and development of a blanching, evanescent, pink
maculopapular exanthem on the neck and trunk. The rash typically lasts approximately 1 2
days. Other associated signs and symptoms include: mild coryza, cough, otits media, headache,
periorbital edema and posterior cervical lymphadenopathy.

Erythematous papules called
Nagayamas spots may be seen on the mucosa of the soft palate and uvula.

Diagnosis is clinical
and treatment is typically supportive.

This is usually a benign and self-limited disease. Febrile
seizures are a common complication. Other potential complications are very uncommon but
include thrombocytopenia, hepatitis, and encephalitis.
Enteroviral Exanthems
Enteroviral exanthems comprise a collection of conditions caused by picornaviruses;
including coxsackievirus, echovirus, and enterovirus. These are the most common summertime
exanthems. Disease expression ranges from exanthems (most commonly seen in younger
children), to aseptic meningitis (older children). The characteristic exanthem is typically
morbiliform. Associated symptoms include upper respiratory symptoms, conjunctivitis, fever,
vomiting, and diarrhea. Complications of this assorted group of viral infections include
pericarditis, myocarditis, pleurodynia, parotitis, hepatitis, pancreatitis, and encephalitis.
One particular enteroviral exanthem caused by coxsackie virus A16 is hand-foot-and-
mouth disease, characterized by oral vesicles followed by vesicles on the hands and feet. Hand-
foot-and-mouth disease has an incubation period of 3 - 6 days. These patients are highly
contagious from 2 days before to 2 days after onset of the eruptions. Hand-foot-and-mouth
disease has a brief prodrome of low-grade fever, malaise, anorexia, and odynophagia. The oral
lesions begin as small red macules that evolve into vesicles ranging from 2 mm 2 cm in
diameter. These vesicles then rapidly rupture, leaving painful erosions. Children often refuse to
eat or drink secondary to the pain; thus, dehydration is a potential complication. The lesions of
the hands and feet begin as macules and papules, then evolve into flat-topped, elliptical vesicles
with an erythematous base. The diaper area may also be affected in infants. Diagnosis is clinical
and treatment is symptomatic. Topical agents such as anesthetic mouthwash may provide relief
from painful oral ulcers. Rare complications include myocarditis, pneumonia,
meningoencephalitis, aseptic meningitis and, as with many of these childhood exanthems,
infection during the first trimester of pregnancy may result in spontaneous abortion.

Disease Season Morphology Distribution Associated findings
Measles Winter
spring
Erythematous
confluent
maculopapular
Begins at hairline,
spreads inferiorly
Kopliks spots, high
fever, 3 Cs
cough, coryza,
conjunctivitis
Scarlet fever Fall spring Generalized
erythema with
Begins on face
and upper trunk
Pastias lines,
exudative pharyngitis,
sandpaper
texture
and spreads
inferiorly
abdominal pain,
rheumatic fever
Rubella Late winter
and early
spring
Rose-pink
maculopapular
Begins on face
and spreads
inferiorly
Lymphadenopathy,
arthralgias
Erythema
infectiosum
Winter and
spring
Slapped cheek,
lacy reticular
rash
Erythematous
cheeks, reticular
extremities
Rash waxes and wanes
over several weeks,
arthritis, aplastic crisis
Roseola Spring Rose-pink
maculopapular
Neck and trunk Lymphadenopathy,
febrile seizures
Varicella Later winter
and early
spring
Vesicles on an
erythematous
base, crusts
Begins on face
and trunk and
spreads
centripetally
Pruritis, varicella
zoster
Coxsackievirus Late summer
or early fall
Ellipitcal
vesicles on
erythematous
base, oral
vesicles and
erosions
Mouth, hands,
feet

Adenovirus Winter
spring
Morbilliform Trunk and
extremities
Upper respiratory
symptoms
EBV Anytime Morbilliform Generalized Hepatosplenomegaly,
lymphadenopathy,
pharyngitis


PETECHIAL RASHES
The most common cause of petechiae is trauma! Caused by coughing, wretching/vomiting!
Petechiae localized to face or head are most commonly cause caused by this mechanism.
2. Henoch-Schonlein Purpura
Henoch-Schonlein purpura (HSP) is a small-vessel vasculitis characterized by purpuric
rash, abdominal pain, arthritis, and hematuria usually seen in children between 3 - 10 years of
age. HSP is often preceded by an upper respiratory infection or drug exposure. The
pathophysiology of HSP involves deposition of immunoglobulin A, C3, and immune complexes
onto small vessels, leading to systemic inflammation. The classic triad associated with HSP
comprises purpura, abdominal pain, and arthritis. The purpura are palpable and most commonly
found in a symmetric distribution over the buttocks and extensor surfaces of the legs. The
abdominal pain is colicky and may be associated with nausea, vomiting, diarrhea, bloody stools,
or intussusception. Hematuria occurs in 10% - 20% of cases; however, less than 1% of children
eventually develop end-stage renal disease. The diagnosis of HSP is clinical, however blood
count, coagulation studies, chemistry, and urine should be collected to exclude other diagnoses
and to evaluate renal function. HSP is a self-limited illness and treatment is supportive.
Nonsteroidal anti-inflammatory drugs may be used to reduce pain in the joints and soft tissue.
Patients should be hospitalized if complications develop, such as significant bleeding,
intussusceptions, or renal failure. Corticosteroids may improve clinical outcomes in severe
hospitalized cases.
3. Meningococcemia
Infection with Neisseria meningitides, a gram-negative intracellular diplococcus, has a
predilection for adolescents and children <4 years old. Meningococcemia is invariably fatal
without treatment. Moreover, mortality remains at 10% 20% even with immediate therapy.
Patients appear ill, febrile, in shock, with mental status changes and a rash that develops within
24 hours of toxicity. The rash is initially erythematous and maculopapular (begins on
extremities) which then spreads and becomes petechial. This is, also, a vasculitic rash with
palpable petechiae. Early in the illness, it can be mistaken for RMSF. Treatment for both is
mandatory for any diagnostic uncertainty. Diagnosis is confirmed by Gram stain and blood and
/ or cerebrospinal fluid (CSF) cultures. Remember, a Gram stain of a meningococcal skin lesion
is more sensitive (72%) than a Gram stain of the CSF (22%). Lumbar puncture, in cases of
meningitis (85% of cases of meningococcemia), classically shows a leukocytosis with neutrophil
predominance, elevated protein, and low glucose. Ceftriaxone is first line therapy, but
vancomycin should be added in cases of diagnostic uncertainty to cover resistant streptococcal
meningitis. Dexamethasone (0.15mg/kg) has been shown to reduce hearing loss and
neurological sequelae if administered early (prior to antibiotics, if possible). Prophylaxis with
rifampin (600mg po BID) is recommended for close contacts (single dose ciprofloxacin 500mg
or intramuscular ceftriaxone 125mg -250mg are alternatives). Vaccination is now recommended
routinely for all 11-18 year olds. Complications include disseminated intravascular coagulation
(DIC), ARDS, renal failure, multi-system organ failure, and adrenal hemorrhage (Waterhouse-
Friderichsen Syndrome).
4. Rocky Mountain Spotted Fever (RMSF)
This is a tick borne illness (Rickettsia rickettsi) that occurs mostly in the Eastern 2/3 of
the United States. The incidence in the United States in 2002 was 3.8 cases / million people.
Unfortunately, only about 50% of patients can recall a tick bite. The erythematous
maculopapular rash classically begins on the wrists and ankles and spreads over the body. Early,
the rash will present as reddish macules that blanch, only to become petechial and purpuric later.
This is a vasculitic rash with palpable petechiae. In up to 20% of cases the rash is absent
(spotless fever). Regardless, the patient will usually be febrile and toxic. The diagnosis is
clinical!! Do not wait for confirmatory antibody tests to begin treatment. Serologic testing will
be negative in the acute period. Lumbar puncture will usually be less dramatic than in
meningococcal meningitis showing a leukocytosis with about 25% neutrophils, elevated protein,
and low to normal glucose. The mortality is approximately 30% if untreated; this decreases to
5% with prompt antibiotic therapy. Doxycycline is the drug of choice in all non-pregnant
patients, even children. Pregnant patients may be treated with chloramphenicol although it
doesnt work as well and you may end up needing to take the risk of using doxycycline in
especially ill patients. Permanent neurological deficits persist in 15% of cases despite optimized
care.
VESICULARBULLOUS RASHES
5. Varicella (Chickenpox)
The incidence of varicella has dropped 90% in the last 20 years, with the introduction and
routine use of childhood vaccinations. Chickenpox, caused by the varicella zoster virus, is
highly contagious and has a peak incidence in late winter and spring. It is seen primarily in
children from 2 - 8 years of age. After an incubation period of 10 - 21 days, the prodrome begins
with malaise, headache, low-grade fever, cough, coryza, anorexia, and sore throat. After
approximately 1 -2 days of prodrome the characteristic skin eruption begins on the trunk and
spreads, over the following week, to the face (including mucous membranes) and extremities
(sparing the palms and soles). The lesions begin as red macules that quickly progress to discrete
vesicles on an erythematous base. The vesicles (commonly described as dew drops on a rose
petal) rapidly evolve into pustules which umbilicate and crust over in 5 - 10 days. The lesions
are intensely puritic. A characteristic feature of chickenpox is crops of lesions, which are
simultaneously present in all stages of development at the same time. The lesions disappear in 7
- 10 days.

The period of infectivity of varicella is from several days prior to the onset of the rash
until all the lesions completely crust over. Diagnosis is typically clinical, but a Tzanck
preparation demonstrating multinucleated giant cells or other viral assays can be used for
confirmation if the diagnosis is unclear.
In most cases, appropriate management of chickenpox is focused on symptomatic relief
of constitutional symptoms and pruritis, as well as prevention of secondary infection.

Wet
dressing, soothing baths, and calamine lotion with oral antihistamines may provide symptomatic
relief of pruritis. Acyclovir may be effective in treating varicella and preventing systemic
complications in immunocompromised children. The role of acyclovir in otherwise healthy
children infected with chicken pox remains unclear.
In normal, immunocompetent children, systemic symptoms are mild and serious
complications are rare. A common complication of varicella includes bacterial superinfection of
the skin lesions.

If present, secondary bacterial infections should be treated with oral antibiotics
directed at Staphylococcus aureus or group A beta-hemolytic streptococci, such as cephalexin,
amoxicillin/clavulanate, or dicloxacillin. If the secondary infection is very localized and minor,
topical mupirocin may also be an option. Other potential complications include pneumonia,
vasculitis, and encephalitis. Immunocompromised children, and those patients receiving chronic
steroid treatment, are more prone to suffer extensive skin eruptions, varicella pneumonia, and
severe constitutional symptoms. Lastly, maternal infection during the first trimester can result in
congenital varicella syndrome, while perinatal maternal infection can result in disseminated
herpes in the neonate.

Perinatal varicella carries up to a 30% mortality; therefore, every effort
should be made to avoid exposure of pregnant women to children with chickenpox.

DIFFUSE ERYTHEMATOUS RASHES
6. Toxic Shock Syndrome
Staphylococcal toxic shock syndrome (TSS) is a potentially lethal disease, which is
characterized by acute onset fever, generalized erythroderma, and hypotension. It is due to a
localized infection or colonization with a toxin-producing strain of S. aureus. While TSS is
classically associated with menstruating women using tampons, recent changes in the
manufacturing and use of tampons has resulted in a decrease in incidence of menstrual-
associated TSS. Currently up to 45% of cases are associated with sources other than tampons,
such as infected wounds. Symptoms characteristically begin with high fever, malaise, chills,
headache, myalgias, vomiting, and diarrhea. Hypotension and multi-organ involvement rapidly
follow. Cutaneous symptoms include a diffuse, blanching, macular eruption, which begins on
the trunk and spreads to the extremities, followed by desquamation, particularly on the palms and
soles. Mucous membranes are involved and may include erythema and ulcerations of the
pharyngeal, oral, conjunctival, or vaginal mucosa. Potential complications include refractory
shock, acute renal failure, neurologic symptoms, DIC, ARDS, and death. Diagnosis is usually
clinical, however occasionally S. aureus may be isolated from localized infection. Rarely
Streptococcus can also cause TSS. The treatment of TSS includes hemodynamic stabilization of
shock and multiorgan failure. Additionally, the physician should attempt to identify and treat the
infection with local drainage if needed or removal of tampon and antistaphylococcal antibiotics.
7. Kawasaki Disease
Kawasaki disease (KD) is an acute, febrile, multi-system illness of unknown etiology,
which causes widespread vasculitis in young children. The incidence of KD peaks at about 9 -
11 months, with approximately 80% of affected children being <5 years of age. The diagnosis
of KD disease can be made if 5 of the following criteria are met:
Fever >39 degrees C for >5 days and 4 of the following:
Bilateral conjunctival injection without exudates
Erythema of the oropharynx, lips with fissures, or strawberry tongue
Acute cervical lymphadenopathy
Polymorphous erythematous exanthem (rash may be morbiliform, scarlantiniform or
maculopapular and may have plaques or target lesions)
Edema of the palms and soles with subsequent desquamation 2 - 3 weeks after onset of
illness
Patients with only four of these symptoms may be diagnosed if coronary aneurysms are found on
echocardiogram. The most important clinical complication is coronary artery aneurysms, which
may lead to myocardial ischemia and sudden death. Other complications are less common and
include hydrops of the gallbladder, diarrhea, small bowel obstruction, arthritis, cystitis, peri- or
myocarditis, valvulitis, and aseptic meningitis. Management of KD is directed at reducing the
risk of coronary artery aneurysm and thrombosis. This is achieved with high dose aspirin and
IVIG. All children with KD should be hospitalized with supportive care.
8. Staphylococcal scalded skin syndrome
Staphyloccocal scaled skin syndrome (SSSS) is a potentially life-threatening, toxin-
mediated disease manifested by tender blistering and widespread desquamation. It usually
occurs in children < 5 years of age. SSSS is postulated to be due to lack of antibodies against
the toxin, and reduced excretion of the toxin as compared to adults. The etiologic agent is
exotoxin-producing Staphylococcus aureus of phage group 2. Initial staphylococcal infection
typically involves the nasopharynx, umbilicus, urinary tract, cutaneous wounds, conjunctiva, or
blood.
Symptoms of SSSS include sudden onset of fever and irritability, followed by slight
diffuse erythema (resembling a sunburn) and cutaneous tenderness (infant does not want to be
held). Symptoms initially affect the perioral and periorbital regions, the neck, axilla, and groin.
This is followed by the exfoliative phase, which involves crusting around the mouth and eyes.
Flaccid bullae develop. Gentle traction on the affected skin results in epidermal separation
(Nikolskys sign), leaving a shiny, moist, red surface. The mucous membranes are not involved.
In the newborn, the entire skin surface may be involved (Ritters disease). The diagnosis is
clinical. Complications may include sepsis and respiratory distress. Treatment is directed
toward elimination of active S. aureus infection, which eradicates the toxin production. Patients
are typically treated with a beta-lactamase penicillin or clindamycin. Although antibiotics are
recommended, it is unclear whether they measurably alter disease course. Hospitalization for
fluid/electrolyte management and for supportive skin care is indicated for most patients.
9. Toxic Epidermal Necrolysis (TEN)

Toxic epidermal necrolysis (Lyell disease) is the most serious cutaneous drug reaction. It is
most commonly associated with sulfa drugs; however, other important triggers include
anticonvulsants, antivirals, non-steroidal anti-inflammatory drugs (NSAIDs), and allopurinol. It
presents as the sudden onset of a diffuse erythema with tender skin and blistering. The skin
cleavage is full-thickness, with positive Nikolskys and Asboe-Hansen signs, and significant skin
sloughing. The Asboe-Hansen Sign (indirect Nikolsky's sign or Nikolsky's II sign) is an
extension of a blister into clinically normal skin with the application of light lateral pressure.
These patients are toxic, with myalgias and significant mucous membrane involvement. These
symptoms occur first on the face (around the eyes), spread caudally to the shoulders and upper
extremities, and then progress to involve the whole body. Women and those with human
immunodeficiency virus (HIV) are predisposed to TEN. Moreover, patients with HIV who are
on chronic trimethoprim sulfamethoxazole prophylaxis and other poly-pharmacy are at 1,000
times greater risk for TEN then those without HIV. Other at risk populations include those with
head injuries, brain tumors, and systemic lupus erythematosus (SLE). The mortality of TEN is
significant, 30% - 35%, even with optimal care. Treatment consists of discontinuation of the
offending agent, wound care, eye care, fluid and electrolyte resuscitation, and intensive care unit
(ICU) or burn unit admission. Intravenous immune globulin (IVIG) may be helpful, although it
is not yet FDA approved for TEN. Ciclosporin is also being studied. Most physicians
recommend against steroid use. Do not use sulfadiazine on the wounds, as sulfa is the most
common offending agent.

10. Erythroderma

Erythroderma, also known as exfoliative dermatitis, is an erythematous, scaling rash that
encompasses 90% or more of the skin. Erythroderma is also termed "red man syndrome" when a
primary cause cannot be identified. The rash begins as a very generalized erythema. Following
the rash, the skin begins to scale and slough; if the sloughing continues, hair loss occurs and nails
become thickened or lost. The skin is inflamed, and may lose pigmenting in dark-skinned
individuals. This is an overwhelming disease process in which large tissue burdens of exfoliated
scales are lost en mass daily; these patients are, in essence, "burn victims." They have marked
increases in skin perfusion and profound temperature dysregulation, resulting in significant heat
loss, increased in basal metabolic rate, fluid loss, edema, and hypoalbuminemia. This is
primarily a disease of adults, but does occur in younger populations when associated with other
skin or connective tissue disorders such as lupus, sarcoid, psoriasis, SSSS, atopic dermatitis, or
seborrheic dermatitis. These patients are quite ill, and will present with fatigue, malaise, fever,
chills, and intense pruritis. History taking is of primary importance, especially as it relates to
other a primary skin disorders, a history of lymphoma or leukemia, drug allergies, and all
prescriptive and over the counter medications. Usually patients presenting with a rapid onset of
symptoms will have a history of cancer, SSSS, or an inciting medication reaction. Those with a
more gradual symptomatology will usually have a history of a previous skin disorder. Many
drugs have been implicated in this disease, including many antibiotics, antihypertensives
(including ace inhibitors), gout medications, anti-fungals, anticonvulsants, non-steroidal anti-
inflammatories, heavy metals, and others. The work up these patients should be in close
consultation with a dermatologist who can aid in the identification of the primary lesions, which
can be a difficult task. Laboratory studies include sedimentation rate, complete blood count,
comprehensive metabolic panel, human immunodeficiency testing, skin scrapings, skin biopsies,
and wound cultures.

Additional studies, directed at detection of an underlying cancer, may be
warranted. Any patient suspected of erythroderma requires admission. Fluids and electrolyte
monitoring is critical. All children with erythroderma and fever must be admitted, as these
findings are predictors of hypotension may reflect toxic shock syndrome. Management includes
skin care, antihistamines, prevention of secondary infections, treatment of the underlying cause,
and topical steroids. Systemic steroids are controversial, and may worsen psoriasis and SSSS.
Recovery is long and recurrences common in the case of red man syndrome. Mortality ranges
from 20% - 40% and in many instances are due to factors unrelated to the disease process itself.


TAKE HOME POINTS
Many pediatric exanthems are benign for children but potentially devastating to
immunocompromised and pregnant individuals.
Rashes with fever deserve extra attention, especially if fever has been present for
more than 5 days.
Palpable petechiae and fever are associated with many types of bacteremia and should
receive intravenous antibiotics immediately.
Patients who are moderately to critically ill with evidence of rash should receive
targeted empirical therapy.
Staphylococcal scaled skin syndrome and toxic shock syndrome require
antistaphylococcal antibiotics, hemodynamic stabilization, and supportive skin care
Drug Reactions: stop the offending agent and all related compounds at once. This
will reduce the risk of death by 30% daily!!
Meningococcemia, and Rocky Mountain Spotted Fever: may present with either
maculopapular (early) or petechial / purpuric rash (late) morphologies. Serial
examinations are mandatory!
Rocky-Mountain Spotted Fever: Doxycycline is the drug of choice, even in
children. Pregnant patients may be treated with chloramphenicol but consider
doxycycline if the patient is especially ill.
Meningitis versus Rocky-Mountain Spotted Fever: If the diagnosis is not clear,
treat both!
Meningitis Prophylaxis: should be given to close contacts. This includes
classmates, household members, and medical personnel who had contact with
respiratory droplets.
Streptococcal Toxic Shock: 80% have an associated skin or soft tissue infection.
Look for it early, as drainage is a critical component of treatment.


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Boguniewica M. Atopic Dermatitis: Beyond the itch that rashes. Immunology and
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