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3년차 이준배
INTRODUCTION
 The emergency physician is more likely to encounter
the life-threatening rashes
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
Erosion
Crust
Ulcer
Lichenification
Excoriation
Atrophy
Head-To-Toe Examination
 Head: patient’s 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-antiinflammatory 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
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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
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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 Nikolsky’s 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)
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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
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1)
2)
3)
4)
5)
the patient is non-toxic and has stable vital signs
the patient is tolerating oral fluids
the rash is not rapidly progressing
the patient is not immunocompromised
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
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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 irritation—neck 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
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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, softtissue 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