3

The emergency physician is more likely to encounter

the life-threatening rashes
INTRODUCTION
Differential Diagnosis And Terminology
Lesion
a general term for a single, small area of skin disease

Rash
the result of a more extensive process and generally involves
many lesions

Transform primary lesions into secondary lesions
various external factors such as scratching, healing,
medications, and infections
Macule
Papule
Nodule
Plaque
Pustule
Vesicle
Bulla
Petechiae
Purpura
Scales
Excoriation
Lichenification
Erosion Ulcer
Crust
Atrophy
Head-To-Toe Examination
Head: patients scalp, conjunctiva, and oral mucosa

Neck: check for nuchal rigidity and other meningeal
signs

Lymph nodes: Adenopathy

Lung: signs of bronchial constriction and edema, such
as tachypnea, wheezing, and retractions
Head-To-Toe Examination
Cardiovascular: heart murmurs (endocarditis)

Abdominal: hepatosplenomegaly (drug
hypersensitivity or viral illness)

Trunk and chest: Most viral exanthems start on the
trunk and then spread to the extremities

Genital: Look in the mucosal areas of the anus and
scrotum or vulva

Head-To-Toe Examination
Extremities: Palpable purpura and petechiae, The
petechial rash of Rocky Mountain spotted fever
spreads from the wrists and ankles

Joints: Arthralgias (sign of serum sickness)

Palms and soles: The classic target lesions of
erythema multiforme are often found on the palms
and soles

Nails and fingers: endocarditis (Splinter hemorrhages
are found under the nails)
Diagnostic Decision Making
Diagnostic Decision Making
Diagnostic Decision Making
Diagnostic Decision Making
Maculopapular Rashes
Cutaneous Drug Reactions
Etiology
The most commonly involved drugs are sulfonamides,
penicillins, anticonvulsants, and nonsteroidal-anti-
inflammatory drugs

Epidemiology
1%-3% of hospitalized patients and 1% of outpatients
Most drug reactions are not serious
The most severe reactions
the hypersensitivity syndrome, Stevens-Johnson syndrome (SJS),
and toxic epidermal necrolysis (TEN)
Cutaneous Drug Reactions
Clinical Presentation
Most cutaneous drug eruptions are morbilliform (meaning it
looks like measles) or exanthematous
Cutaneous Drug Reactions
Diagnosis
clinical
Cutaneous Drug Reactions
Cutaneous Drug Reactions
Cutaneous Drug Reactions
Treatment
Removing the drug
If possible, all drug therapy should be stopped
Routine use of corticosteroids is not indicated
Oral antihistamines (diphenhydramine 25-50 mg PO q6h prn)
may alleviate pruritus
Erythema Multiforme, Stevens-Johnson Syn
drome, And Toxic Epidermal Necrolysis
Erythema Multiforme
Etiology
EM is a common acute inflammatory disease that is usually
self-limited
in up to 50% of cases no etiologic agent can be identified
Erythema Multiforme
Erythema Multiforme
Pathophysiology
Not clearly understood

Epidemiology
The true incidence of EM is not known

Morbidity And Mortality
Rare
If patients have ocular involvement, disabling and permanent
visual sequelae may occur
Erythema Multiforme
Clinical Presentation
Chief complaint : rash
malaise, fever, and arthralgias
Target lesions are the hallmark of EM minor and major
EM minor
mucous membrane involvement is absent
bullae and systemic symptoms do not develop
becomes EM major if a single mucous membrane is involved
Erythema Multiforme
Diagnosis
Clinical
classic target lesions
if the patient looks toxic, has systemic complaints, or has
abnormal vital signs, consider an alternative diagnosis
Erythema Multiforme
Management
EM minor and major generally resolve without treatment in
2-3 weeks
underlying infection should be treated
Based on a review of the literature, there is no strong
evidence that steroids are beneficial in EM minor or major
systemic antihistamines and possibly analgesia
Erythema Multiforme
Disposition
All patients diagnosed with EM minor or major can be safely
discharged home
Follow-up with the primary medical doctor or dermatologist
Patients must return to the ED if there is rapid progression
Follow-up with an ophthalmologist
Vesiculo-Bullous Rashes
Stevens-Johnson Syndrome (SJS) ,Toxic Epidermal
Necrolysis (TEN), and pemphigus vulgaris (PV)
Potentially life-threatening
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Etiology
SJS and TEN are related to the use of certain medications

Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Pathophysiology
Not completely understood

Epidemiology
0.4-1.2 cases per million per year
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Morbidity And Mortality
The leading causes of death in TEN are sepsis from
Staphylococcus aureus or Pseudomonas aeruginosa and
fluid/electrolyte abnormalities
The mortality rate
5%-10% for SJS
23%-30% for TEN
Higher in elderly
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Morbidity And Mortality
Variables associated with a poor prognosis
increased age, extent of disease, extent of disease at time of
transfer to a burn center, azotemia, multiple medication use,
thrombocytopenia, and neutropenia
Ophthalmologic sequelae
keratitis and corneal ulcerations, cornel scarring
blindness occur in 40%-50% of patients
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Clinical Presentation
Rash, myalgias, fever, cough, or sore throat
If a new drug is the cause, the prodrome usually begins
within days of ingestion
Skin lesions then develop suddenly, after 1-2 weeks of
prodromal symptoms
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Clinical Presentation
SJS
atypical target lesions or purpuric macules on the trunk
oropharyngeal lesions causing an erosive stomatitis
purulent conjunctivitis can lead to ocular erosions and blindness
SJS is a selflimited disease
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Clinical Presentation
TEN
skin tenderness, pruritus, and pain
Onset is more rapid with repeated ingestion of the inciting
agent
warm and tender erythema that first affects the face around the
eyes, nose, and mouth
Lateral pressure on normal skin adjacent to a bullous lesion
dislodges the epidermis (This is known as Nikolskys sign)
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Clinical Presentation
The clinically distinguishing features of SJS and TEN is the
degree of epidermal detachment
SJS involves mucosal erosions and less than 10% of epidermal
detachment
TEN is defined by more than 30% of epidermal detachment
Between 10%-30% is considered the overlap zone of SJS and
TEN
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Diagnosis
Clinical
Biopsy
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Treatment
supportive
removal of the offending agent
replacement of fluid losses
similar to burn victims
analgesics
all drugs started within the past month should be
discontinued
avoid Silvadene (silver sulfadiazine)
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Treatment
the role of corticosteroids in SJS and TEN is highly
controversial
Based on a review of the literature, there does not appear to be
a consensus on the use of steroids in the treatment of SJS and
TEN
aseptic technique to avoid infection
use of adhesive material, ointments, and creams should be
avoided
Patients should be covered in a clean white sheet
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Treatment
Debridement of necrotic tissue may be necessary
Prophylactic antibiotic therapy is no longer given
Crossreactivity with the drug that initiated the TEN
the risk of selecting for resistant organisms
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Disposition
Some patients diagnosed with SJS can be safely discharged
from the ED
1) the patient is non-toxic and has stable vital signs
2) the patient is tolerating oral fluids
3) the rash is not rapidly progressing
4) the patient is not immunocompromised
5) close follow-up is ensured
Ophthalmologist f/u
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Disposition
If these criteria are not met, patients with SJS should be
admitted
24-hour observation
IV hydration
local skin care
nutritional support
If there is any progression of lesions, transfer to a burn or
intensive care unit should be considered
Stevens-Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TEN)
Disposition
All patients suspected of having TEN should be admitted to
an intensive care unit
early transfer to a burn unit may be necessary
patients who were treated in a burn unit had lower rates of
bacteremia, septicemia, and mortality if transfer was done early
in the hospital course (less than seven days)
Pemphigus Vulgaris
Etiology
rare but potentially lethal
autoimmune disease
Erosions and blistering of epithelial surfaces of the oral
mucosa and skin

Epidemiology
4500 cases a year
Pemphigus Vulgaris
Pathophysiology
circulating IgG autoantibodies that bind to the surface of the
keratinocytes
blisters form within in the epidermal layer of the skin
Pemphigus Vulgaris
Clinical Presentation
Initially, blisters localize to the oral mucosa weeks to months
before the skin blisters appear
Over several weeks, non-pruritic skin blisters erupt over the
rest of the body
head and trunk first
Ruptured blisters develop into painful erosions that may
become secondarily infected
Pemphigus Vulgaris
Clinical Presentation
the mortality is approximately 10%-20%
Most of the complications are due to infections
Some patients can develop extensive fluid, protein, and
electrolyte loss in association with extensive blistering
Pemphigus Vulgaris
Diagnosis
Biopsy
Immunofluorescence demonstrates IgG on the surface of
keratinocytes
emergency physician must act based on the clinical scenario
Pemphigus Vulgaris
Pemphigus Vulgaris
Treatment
A low daily dose of prednisone (1 mg/kg/d) is the initial
treatment
Steroids are given until remission
no new blisters for one week
Most cases of PV can be treated at home as long as the
patient is not toxic-appearing and has only a few blisters
Pemphigus Vulgaris
Treatment
Patients with extensive blisters, erosions of the skin, or who
are toxic-looking should be admitted
monitored and treated for fluid or electrolyte imbalances and
observed for potential infection
if there are overt signs of infection in the ED, start antibiotics
immediately
Petechial/Purpuric Rashes
Meningococcemia
Neisseria meningitidis

colonization of the nasopharynx and then progress to
systemic invasion
bacteremia, sepsis, CNS invasion

Untreated, meningococcemia is invariably fatal
Even with prompt treatment, the mortality rate is about
10%-20%
Meningococcemia
Clinical Presentation
usually begins 3-4 days after exposure
fever, chills, malaise, myalgias, headaches, nausea, and
vomiting
A rash is seen in more than 70% of people with
meningococcemia
Petechiae, which develop on the wrist and ankles
Look for signs of meningeal irritationneck soreness or
stiffness, photophobia, and headaches
Meningococcemia
Clinical Presentation
septic shock, with acute renal failure, hypoxia, hypotension,
multi-organ failure, and disseminated intravascular
coagulopathy
Early diagnosis and treatment are crucial
Biopsy and Gram stain

Meningococcemia
Meningococcemia
Treatment
Ceftriaxone (2 g q12h)
bacterial causes of purpuric disease
N. meningitidis, H. influenzae, and S. pneumoniae
IV penicillin G (4 million units q4h)
ampicillin (2 g q6h)
In cases of severe penicillin allergy, IV chloramphenicol 4 g/d
is indicated
Meningococcemia
Treatment
Supportive care involving IV fluids is crucial in the patient
with overt or incipient shock
Close contacts, such as daycare center personnel, household
members, or ED personnel
antibiotic prophylaxis
ciprofloxacin 500 mg PO
rifampin 600 mg q12h PO for two days or ceftriaxone 250 mg
IM
Rocky Mountain Spotted Fever
Rickettsia rickettsii
the bites of several species of ticks

The mortality rate for the untreated exceeds 30%
Risk factors for mortality include delay in treatment and
advanced age

Rocky Mountain Spotted Fever
Clinical Presentation
The rash typically appears on the fourth day after the bite
(range, 1-15 days)
erupting first on the wrist and ankles
In severe cases of RMSF, multiple organs can be involved
CNS involvement may range from headaches (very common) to
coma and even seizures
Disseminated intravascular coagulopathy is a predictor for
mortality
Rocky Mountain Spotted Fever
Clinical Presentation
The diagnosis of RMSF is empiric and is initially based on
clinical and epidemiologic findings
triad of fever, rash, and a history of tick bite
Rocky Mountain Spotted Fever
Treatment
Adults : doxycycline 100 mg BID PO or IV for seven days or
for two days after temperature has normalized
Young children
Chloramphenicol or doxycycline
pregnant women
chloramphenicol 500 mg QID PO or IV for seven days or for two
days after the temperature has normalized
Rocky Mountain Spotted Fever
Treatment
The need for hospitalization depends on the severity of the
illness
Long-term sequelae
hearing loss, peripheral neuropathy, bladder and bowel
incontinence, and cerebellar, vestibular, and motor dysfunction
Diffuse Erythematous Rashes
The differential diagnosis for diffuse erythematous
rashes is broad

rapidly lethal
the toxic shock syndromes (TSS)
necrotizing fasciitis
Staphylococcal Toxic Shock Syndrome (TSS)
and Streptococcal Toxic Shock Syndrome
(STSS)
Etiology
exotoxin-mediated diseases
fever, rash, mucous membrane involvement, and
hypotension

Pathophysiology
colonization of toxin-producing strains of S. aureus
Staphylococcal Toxic Shock Syndrome (TSS)
and Streptococcal Toxic Shock Syndrome
(STSS)
Epidemiology
In TSS
young, healthy women who used hyper-absorbent tampons
vaginal colonization of toxin-producing strains of S. aureus
increased patient and physician awareness, along with removal of
these tampons from the market, has decreased the incidence of
TSS in menstruating women
Staphylococcal Toxic Shock Syndrome (TSS)
and Streptococcal Toxic Shock Syndrome
(STSS)
Epidemiology
In TSS
abscesses, bursitis,surgical wounds, indwelling foreign bodies
such as nasal packing, and in post-partum patients
In STSS
soft-tissue infection or minor skin trauma
Staphylococcal Toxic Shock Syndrome (TSS)
and Streptococcal Toxic Shock Syndrome
(STSS)
Morbidity And Mortality
the morbidity and mortality are higher in STSS than TSS
shock, renal failure, sepsis, and adult respiratory distress
syndrome
The overall mortality is 30%, and mortality rates can reach
80% in the elderly
Staphylococcal Toxic Shock Syndrome (TSS)
and Streptococcal Toxic Shock Syndrome
(STSS)
Clinical Presentation
low-grade fever, malaise, myalgias, and vomiting
Symptoms may occur within 2-3 days of tampon use, soft-
tissue infection, or within a week of other inciting factors
high fever, rash, and hypotension begins abruptly after the
prodrome

Staphylococcal Toxic Shock Syndrome (TSS)
and Streptococcal Toxic Shock Syndrome
(STSS)
Clinical Presentation
Hypotension develops rapidly, leading to tissue ischemia and
subsequent multisystem involvement
Rash is a characteristic feature of TSS
usually develops 1-3 days after other major symptoms
If the patient is thrombocytopenic, purpura may develop
Staphylococcal Toxic Shock Syndrome (TSS)
and Streptococcal Toxic Shock Syndrome
(STSS)
Clinical Presentation
A key distinguishing factor of STSS, present in 85% of
patients, is extreme localized pain at the site of infection that
is out of proportion to physical findings
Staphylococcal Toxic Shock Syndrome (TSS)
and Streptococcal Toxic Shock Syndrome
(STSS)
Diagnosis
Clinical
TSS





STSS
Soft-tissue infection
may progress to
necrotizing fasciitis or myositis

Staphylococcal Toxic Shock Syndrome (TSS)
and Streptococcal Toxic Shock Syndrome
(STSS)
Staphylococcal Toxic Shock Syndrome (TSS)
and Streptococcal Toxic Shock Syndrome
(STSS)
Treatment
Aggressive resuscitation
vasopressors, inotropic agents, and mechanical ventilation
In TSS, remove the source of staphylococcal colonization,
such as vaginal tampons, nasal packing, or breast implants
Staphylococcal Toxic Shock Syndrome (TSS)
and Streptococcal Toxic Shock Syndrome
(STSS)
Treatment
In TSS, antibiotic therapy with anti-staphylococcal coverage
is recommended
oxacillin, nafcillin, cefoxitin, vancomycin, or clindamycin
decrease the rate of recurrence
The use of steroids in TSS and STSS is controversial
Staphylococcal Toxic Shock Syndrome (TSS)
and Streptococcal Toxic Shock Syndrome
(STSS)
Treatment
In STSS, antibiotic treatment is essential
broad-spectrum antibiotic coverage
penicillin G or ampicillin, plus clindamycin, and possibly an
aminoglycoside
Staphylococcal Toxic Shock Syndrome (TSS)
and Streptococcal Toxic Shock Syndrome
(STSS)
Disposition
All patients who are suspected of having TSS or STSS should
be admitted