Skin and dermatology emergency

1. Adib Mursyidi Iskandar Mirza
A&E Department

2.  Must know:
 How to describe rashes
 Basic differential diagnosis
 Toxic vs. non-toxic rash
 Basic management/resuscitation
 When/how to talk to your consultant
 Why important?
 5% All ED visits

5.  Morphology
 Arrangement
 Distribution/Pattern
 Extent
 Evolutionary Change
GOAL : NOT for INSTANT DIAGNOSIS 
purpose to detect toxicity and categorize the
rash

7.  Goal: Improve how we think about rashes
and categorize them in our minds :
 Question 1: Rash morphology
 Question 2: Rash Distribution/Pattern
 Question 3: Sick or not Sick

8.  The Red Flags are based on
 History
 Vitals are vital
 Labs

15.  Secondary Syphilis
 Anthrax
 Vitiligo
http://manbir-online.com/grafics/Syphilis-hands.jpg

17.  Bacterial Folliculitis
 Gonorrhea
 Generalized pustular
 Psoriasis
http://www.dermnetnz.org/acne/img/s/folliculitis5-s.jpg

19.  Acute inflammatory skin disease
 Strike all ages : highest in young adults (20-
40)
 More often in females, common in spring and
fall

20.  Mild papular eruption 
diffuse vesicobullous
lesion + mucus
membrane involvement
and systemic toxicity
 Precipitating factors:
infection
(mycoplasma/herpes
simplex), drugs
(antibiotic/anticonvulsio
n) and malignancy

21.  Malaise/atralgia, fever,
generalized burning
sensation, pruritus
 Initial lesion :
erythematous papules
 follow by target
lesion in 24-48h

22.  Target lesion : high
suggestive for EM
 Present of mucosal
involvement suggest
of EM major

23.  Patient without systemic manifestation and
mucous membrane involvement 
outpatient + dermatologic consultation
 Systemic steroid burst (Prednisolone 60-
80mg OD)
 Extensive disease or systemic toxicity require
critical care + fluids management

24.  Related to the use of medications (NSAID,
antibiotics, anticonvulsant, sulfonamides)
 Leading cause of death : SEPSIS
(staphylococcus aureus/pseudomonas
aeruginosa), fluids and electrolyte abnormality
 Mortality rate: 5-10% (SJS), 23-30% (TEN)

25.  Chief complaint : RASH
 Prodromal symptoms: Malaise, anorexia,
myalgia, arthralgia, fever, URTI
 If causes are drugs  usually begins within
days of ingestion

26.  SJS
 Atypical target
lesion/purpuric macules
on trunk
 Common develop
oropharyngeal lesions 
causing erosive
stomatitis
 Purulent conjuctivitis
leads to ocular
erosion/blindness
 TEN
 Complaint of skin
tenderness, pruritus, pain
 Onset : rapid with
ingestion of agent
 Warm, tender erythema
that affects the face
around eyes, nose, mouth
 Then extends to
shoulders and trunks in
symmetric fashion
 Nikolsky sign +ve

27.  Clinically distinguishing features of SJS and TEN
 degree if epidermal detachment
 Stevens-Johnson syndrome: A minor form of
toxic epidermal necrolysis, with less than 10%
body surface area (BSA) detachment
 Overlapping Stevens-Johnson syndrome/toxic
epidermal necrolysis: Detachment of 10-30% of
the BSA
 Toxic epidermal necrolysis: Detachment of more
than 30% of the BSA

29.  Treatment is supportive
 Management : focus on removal of offending
agent and fluids loses replacement
 Analgesia, corticosteroid (controversial)
 Require aseptic techniques when handling
 Debridement of nectrotic tissue may be
needed later

30.  Autoimmune disease, characterized by
erosion and blistering of epithelial surfaces of
the oral mucosa and skin
 Mean age of 6th
decade
 PV can lead to significant morbidity (due to
pain and disfigurement) and mortality (due to
loss of protective barrier and secondary
infection)

31.  Initially blisters localize to
the oral mucosa weeks to
months before skin blister
appears
 Non pruritic skin blisters
erupt over the rest of body
(size from 1cm to several
cm)
 Ruptured blisters develop
into painful erosion
become secondary
infection
Early, small blister filled with
clear fluid arises on healthy skin.

32. Flaccid blister filled with clear fluid
arises on healthy skin.
Erosion

33. Erosions and healing areas on the back

34.  Skin biopsy
 In ED practical : based on clinical scenario
 Treatment: low daily dose of prednisolone
(1mg/kg/d) is the initial  given until
remission (define as state of no new blisters
for 1week)
 If new lesion appear after 1-2weeks of
treatment  increase the dose of steroid

35.  Causes by Neisseria meningitidis (gram –ve
diplococcus)
 Begin with colonization of the nasopharynx
and progress towards systemic invasion 
leading to bacteremia, sepsis/CNS invasion

36.  Incubation period 2-10days, usually begins 3-
4days after exposure
 Fever, chills, malaise, myalgias, headache,
nausea, vomiting
 Rashes seen in 70% with meningococemia

38.  In cases organism not yet identified :
ceftriaxone (2g BD) is the choice
 Supportive care (IV Fluids, isolation)
 Closed contact with the patient  antibiotic
prophylaxis (ciprofloxacin 500mg PO)

39.  Differential diagnosis is broad
 Examples: viral exanthema, staphylococal
scalded skin syndrome, Kawasaki disease,
necrotising fasciitis, TSS/STSS

40.  Staphylococcal Toxic Shock Syndrome (TSS)
 Strepptococcal Toxic Shock Syndrome
(STSS)
 Both had similar etiology, clinical
presentation and treatment
 TSS is cause by colonization of toxin
producing strain of S. aureus
 STSS cause by local tissue invasion of the
infecting organism S. pyogenes

41.  TSS: common in female during discovered
85-90% cause by the usage of tampons 
vaginal colonization of toxin producing
strains of S. aureus
 STSS: 20-50% occurred in 20-50 years old
 80% associated with soft tissue
infection/minor skin trauma  most likely to
develop bacteremia

42.  Prodrome of low grade fever, myalgias,
vomiting (minor symptoms)  2-3 days after
the inciting factors
 Major symptoms : high grade fever, rashes,
hypotension  begins after prodrome
symptoms

43.  Rashes: diffuse, non pruritic, blanching,
macular erytroderma
 Generally erupts on the trunk  most
prominent
 Full thickness desquamation of the palms and
soles occurs 5-13 days after the onset

44.  Both STSS/TSS requires presence of high
fever, rash followed by desquamation, mucus
membrane involvement, 3 or more organ
systems

46.  Resuscitation (inotropes supports, fluids,
ventilations)
 Removal of the sources (tampons, nasal
pack)
 Antibiotic :
 TSS: IV Beta Lactamase resistants (oxacillin,
vancomycin, clindamycin)
 STSS: broad spectrum coverage until specified
organism identified
 Infection site cultures

47.  Have a systematic, simple approach to the
unknown rash
 Diagnosis of rashes  clinical and physical
exam findings outweigh lab evaluation
 Need careful history : immune status, recent
medications, where rashes started, presence
of associated symptoms
 Need to recognize potentially lethal
condition and level of toxicity

48.  References
 Nguyen T., Freedman J. Emergency Medicine
Practice Bulletin. Dermatologic Emergencies:
Diagnosing and Managing Life-Threatening
Rashes. September 2002.
 Tintinalli’s Emergency Medicine. 7th
Edition.
 Emergency Medicine : Sherley Ooi 2nd
Edition