Dermatologic Emergencies
History
It is important to establish the onset of the first lesion. The location and
description of the first lesion may be helpful in determining the cause of the rash. Then
the pattern and distribution of subsequent lesions should be established. Are the lesions
transient, do they migrate? It is also important to ask about blisters, vesicles,
discharge, ulcerated and weeping areas. It is also important to determine whether or not
the rash is itchy. This can be followed by a general medical history followed by
exposures, travel, sexual history and immunization history. Finally, enquire about meds
including otc and alternative meds and allergies
Physical Exam
Assess vitals
Examine the rash: examine in good light, disrobe patient
Distribution: Generalized vs Localized
Generalized rashes: usually secondary to internal/systemic exposuredrugs, viruses
Localized: local exposure (however some systemic illnesses manifest as
local rashes i.e. lupus, HSP)
Pattern- location, symmetry, configuration
Anatomical location – scalp, face, mouth, trunk, axilla, perineum, limbs,
palms and soles
Symmetry (systemic exposure) vs Asymmetry (local exposure)
Configuration – relationship of lesion to other lesions
Types of Primary lesions
Macule
flat circumscribed discolored lesion <1cm
Patch
flat, circumscribed discolored lesion >1cm
Purpura
flat non-blanching discoloration of skin
Abscess
tender erythematous fluctuant nodule
Nodule
raised palpable solid nodule <1cm
Tumor
raised palpable solid nodule >1cm
Wheal
transient edematous papule/plaque w/ erythema
Vesicle
thin walled circumscribed blister <5mm
Bulla
thin walled circumscribed blister >5mm
Pustule
vesicle with pus
Papule
raised solid palpable lesion < 1cm
Plaque
raised solid palpable lesion > 1cm
Secondary lesions: scar, erosion, excoriation, fissure, ulcer, telangiectasia
Diagnostic Tests- in Tintinalli but not that practical
-KOH test- place lesion on slide with 20% KOH and examine for hyphae
-Scabies and Lice- scrape specimen onto slide, add drop of mineral oil and examine
under microscope
-Tzanck smear: unroof blistering lesions (HSV)
-Woods light: UV @ 365 nm : Erythrasma – red Tinea Versicolor – green/yellow
GENERAL TREATMENT MEASURES
1) If its wet- dry it. If its dry, wet it
2) Oral steroids- urticaria, angioedema, toxicodendron dermatitis
a. Use in caution in diabetes, PUD, immunodeficiency and some psychiatric
disorders
3) Topical steroids – 7 groups based on vasoconstriction. Fluorinated are stronger,
but avoid in pregnancy. Group 7 is weakest i.e. 1 and 2.5% hydrocortisone cream
and group 1 is strongest i.e. betamethasone. clobetasol
4) Oral antihistamines
5)Antimicrobial agents – topical vs oral
a. Antibacterial
b. Antifungal- clotrimazole, miconazole, ketoconazole
c. Antivirals – acyclovir
d. Anti-infestation – premethrin, lindane (don’t use in small kids, may cause
neurotoxicity)
10 Life Threatening and Serious Skin Disorders
1) ERYTHEMA MULTIFORME - Definition: hypersensitivity reaction with
immunoglobulins and complement component deposition in the cutaneous microvascular.
Spectrum of disease: minor (localized papules) to major (generalized vesiculobullous
lesions and mucous membrane erosions)
Who gets it: More common in males, most common age 20-40
What causes it:1) Idiopathic
2) Infections: Viral- many viruses but HSVI and II are most common, also
many bacterial causes- mycoplasma pneumonia is most common
3) Drugs: antibiotics and anticonvulsants
Prodrome of fever malaise, myalgia, arthralgias 1-2 weeks prior to onset. Skin burning
Characteristic lesions: Maculopapular lesions, target lesions, vesiculobullous lesions on
extensor surfaces and mucosal surfaces. Centripetal spread
Minor- target lesions/ raised edematous papules, acral distribution
Major- same as minor but 1 or more mucous membranes involved. Epidermal
detachment usually less than < 10% TBSA.
Mucous membrane involvement usually oral and usually not as severe as SJS/TEN
Complications: fluid and electrolyte imbalances, secondary infections
Treatment
1) Short course of prednisone 60-80mg 2) Analgesics 3) Antihistamines
4) Antibiotics
May require ICU
Close to 0% mortality with resolution at 2-4 weeks without consequence
2) Toxic Epidermal Necrolysis/SJS
Similar etiology and prodrome as EM but more likely drug related, more mucous
membrane involvement (eyes, esophagus, airway, ano/genital), more likely to have
central lesions, with more hemorrhagic bullae. Histiologically differs from EM
Who gets it: all ages, both genders
What causes it: 1) Idiopathic,
1) Drugs antibiotics ( pcn, sulfa), anticonvulsants, oxicam/ NSAIDs,
2) Infections: Viral HSV and HIV, bacterial infections
3) Malignancies
Characteristic Lesions: Warm tender erythematous skin progresses to vesicles, bullae
with mucous membrane involvement and eventual exfoliation
Nikolsky sign: touching skin adjacent to bullous lesion results in dislodgement of skin
(epidermis from dermis). Large areas of denuded dermis
SJS < 10%TBSA epidermal detachment,
Between 10=30% BSA is considered overlapping SJS/TEN
TEN > 30% TBSA epidermal detachment.
Complications:
Infection
Hypovolemia
Perilabial and airway sloughing
Ocular involvement: conjunctivitis, conjunctival erosions, eye edema
Management: ICU or Burn Unit
burns protocol,
IV rehydrate,
remove offending agent.
Consider IVIG and optho consult for eye involvement
Mortality: SJS has 5% mortality, TEN 30% mortality
3) Exfoliative Dermatitis ( Erythroderma)
Erythematous rash involving 90% of the skin that progresses to diffuse exfoliation
Who gets it: all ages, more common in males ( 2:1) and age > 40
What causes it: 1) Preexisting skin disease (10-40%): eczema, psoriasis
2) Malignancies (10-40%)- lymphoma, leukemia, MML, carcinomas,
paraneoplastic syndrome
3) Drugs (3-10%)
4) HIV
5) Idiopathic
Characteristic Lesion: Warm erythematous skin. Initially burning and itching that
progressives to generalized exfoliation.
Complications: fluid loss, hypothermia, infections
Management: withdraw offending agent, treat underlying condition, replace fluids. May
need ICU or burn unit
Mortality: 30%
4) Disseminated Gonococcal infection
Disseminated gonococcal infections follow 1-2% of GU/mucosal infections with N
gonorrhoeae. Joint pain ( arthritis/tenosynovitis) with a rash
Who gets it: sexually active adults, more common in females
What causes it: disseminated N gonorrhoeae infections
Prodrome: Preceding mucosal infection followed by fever, arthralgia, tenosynovitis but
may not be systemically unwell and primary infection likely absent by this time
Characteristic Lesion: 5-40 lesions- multiple papular vesicular and
pustular/hemorrhagic skin lesions on extensor surfaces of wrist, palms, ankles, feet. May
be petechial w/ necrotic centres.
Complications: septic arthritis ( knee most common), meningitis, endocarditis
Treatment: Ceftriaxone
Mortality: low
5)Meningococcemia
Initially maculopapular or petechial rash that rapidly progresses to prupura, bullae,DIC,
shock and death caused by Neisseria Meningitidis
6) Toxic Shock Syndrome
Severe syndrome with high fever, diffuse erythroderma, mucousmembrane hyperemia,
pharyngitis, GI upset associated with staph infection. Similar but rarer STSS (Strep
Toxic Shock Syndrome assoc with GAS)
Major criteria
Fever: temperature >38.9°C (102°F)
Rash: diffuse macular erythroderma (sun burn) followed by desquamation: 1 to 2
wk after onset of illness, particularly of palms and soles.
Hypotension: systolic blood pressure <90 mm Hg for adults or <5th percentile by
age for children <16 yr of age, or orthostatic syncope, orthostatic drop > 15mmHg
Mucous membrane hyperemia
Multisystem organ failure- 3 other systems: MSK, GI, Renal failure, ARDS,
CNS
Who gets it: More common in women (90%) but can effect all ages.
What causes it: Staph infections that produce the exotoxin TSST-1 Previously more
common in tampon users. Menstrual related TSS remains somewhat common. Other
causes include diaphragms, sponges, nasal packing, body piercing, post op
Prodrome: malaise, myalgia, headache, n&v, diarrhea.
Complications: numerous
Treatment
Stabilise and remove potential sources of infection
anti-staph agents suggested but do not alter course of disease (decrease recurrences)
7) Staph Scalded Skin Syndrome
Staph producing exotoxin (exfoliatin) that cleaves skin within epidermis. More
superficial then TEN
Who gets it: mostly kids under 5
What causes it: staph exotoxins
Prodrome: clinically occult staph infection of eyes, naso pharynx or umbilicus
Characteristic lesions: Begins around the mouth and leads to erythematous skin (stage
1) followed by exfoliation (stage 2, day 2) and with desquamation and bullae (stage 3 on
days 3-5). Nikolksy positive
Treatment: Penicillinase resistant antibiotic (Clox or Vanco), fluid replacement
8) Bullous disease
Pemphigus Vulgaris- generalized mucocutaneous autoimmune blistering eruption.
Begins as clear flaccid fragile blisters. Nikolsky positive. Autoimmune reactio to
desmolgein- glue that holds epidermal cells together
95% mucous membrane involvement
Who gets it: ages 40-60 but can occur in all ages
Treatment- fluid and steroids
Bullous pemphigoid- More benign and usually self limited, disease of elderly
deeper into dermis therefore blisters are more tense and larger. May begin as hives.
Autoimmune reaction to collagen
Who gets it: mostly elderly
Treatment- fluid and steroids, minocycline or tetracycline, immunosuppresors if severe
Pemphigoid Gestationalis- associated with pregnancy
9) Rocky Mountain Spotted Fever
Tick born bacteria Rickettsia ricketsii, potentially fatal multisystem disease from
necrotizing vasculitis
Who gets it: all ages, more common on East Coast
What causes it: see above. People in close proximity to deer, cattle, pets, rodents
Prodrome: constitutional symptoms up to 1 week after exposure. Classic triad is fever,
rash with tick exposure
Characteristic lesion: discrete maculopapular blanchable lesions that first appear on
wrist and ankles. Evolves into petechiae
Complications: hepatosplenomegally, meningismus, renal and hepatic failure,
myocarditis. 50% mortality if untreated
Treatment: doxy
10)Angioedema
Well-circumscribed areas of edema caused by increased vascular permeability. Usually
presents as acute swelling of face, extremities or genitals. Also may have abdo pain and
airway compromise
Who gets it: all ages
What Causes it:
1)Meds- AceI, pcn, NSAIDs, contrast material
2)Food allergens
3)Physical agents- trauma, friction, cold
4) C1 Esterase Inhibitor Deficiency- low levels of C1-INH
a) hereditary ( autosomal dominant)
b) acquired ( autoimmune disorders and B cell malignancies)
Complications: airway compromise, unnecessary abdominal surgeries, peripheral edema.
To assess for airway compromise in these patients, watch for difficulty swallowing
secretions and a change in voice. Peripheral edema is not pitting, non erythematous and
no hives. Usually unilateral and may be associated with minor trauma.
Treatment
If you can’t distinguish between this and anaphylaxis- treat for anaphylaxis
Antifibrinolytics (Amicar)- for acquired only
Anabolic androgens ( danasol)- increase C1- INH
Plasma derived C1-INH (Berinert)- self-administered
FFP if Berinert not available
Infestations
1) Scabies
Definition: itchy polymorphic rash commonly of hands and feet
Who gets it: Common in children, low SES, immunocompromised
What causes it: Sarcoptes Scabiei T
Prodrome: takes 3 weeks from infection to onset of symptoms
Characteristic lesion: burrow- red linear line or S shaped with central scale
a. Crusted scabies: large mite burden leading to less itchy but thick
hyperkeratosis of hands and feet. Highly contagious
Treatment: premethrin 5 % or lindane 1% lotion left on overnight, wash clothes in hot
water, treat contacts and repeat treatment in 1 week
2) Lice
Definition: pediculosis capitis = head lice, pediculosis corporis = body lice,
pediculosis pubis = crabs)
Who gets it: same as scabies
What causes it: see above
Prodrome: Itchiness in affected area
Characteristic lesion: white nits in hair, may see lice clinging to hair shafts
near scalp
Ova or nits are adherent to hair shaft and if > 1cm from skin, have likely
hatched (need to remain close to scalp because they feed off blood)
Treatment: Nix (premethrin 1%) rinse for 10 min, nits can be removed with 50% vinegar
solution applied to hair followed by combing with fine toothed comb
Rashes of Groin
Tinea Cruris (Jock itch)
Definition: Fungal rash involving the groin
Who gets it: all ages, more common in males
Characteristic lesion: erythema with slightly raised scaly edge, may extend to
thighs but spares the penis and scrotum
Treatment: topical antifungal i.e. clotrimazole, ketoconazole. Consider
polysporin to prevent bacteria super infection. Spectazole has antifungal and
antibacterial properties. May require oral antifungals
Erythrasma
Infection caused by Corynebacterium minutissimum. Commonly in groin. Treated with
erythromycin. Will illuminate with woods lamp
Rashes on Face and Scalp
Erysipelas and cellulitis– hot red rash on face. Erysipelas more superficial then
cellulitis. Caused by GAS and staph
Treatment: Keflex
Herpes Simplex I- cold sores (herpes labialis).
Treatment antiviral or antiviral ointment ( penciclovir, Zovirax)
Herpes Zoster
May involve any of the branches of the trigeminal nerve. V1 (ophthalmic branch) with
lesions of nose (Hutchinson’s sign) may have associated keratitis. Keratitis responds to
ocular steroids. May also cause Ramsay Hunt syndrome (lesions in auditory canal) or
Bell’s Palsy.
Treatment: antivirals (acyclovir 800mg po 5/day for 1 week, Valtrex 1 g po tid x 1 week,
famvir 500mg po tid x 1 week. Refer to ophthalmology if needed
Lupus- discoid or malar rash
Tinea Capitus
Superficial infection caused by dermatophytes
Annular configuration with erythema and scaling
Treated with antifungals
If not improving think secondary infection
Rashes of Skin Folds
Candida Intertrigo
Bright red rash with satellite papules and pustules moist chronically occluded
areas. Predisposing factors include antibiotics (topical or oral), steroids,
immunocompromised states, obesity. Non infectious intertrigo may also be a result of
irritation from moisture, heat and friction. Urine and Feces may also cause non infectious
intertrigo
Diagnosis: KOH slide prep
Treatment
Topical antifungals, drying agents (Zeasorb AG), astringent agents (Burow
solution), keep the area dry
Rashes of lower extremities
Lichen Simplex Chronicus
Itchy well demarcated hyperpigmented plaques. Affects ankles, shins and feet. May also
affect groin. Need to rule out fungal infections
Treatment; stop the itch and high potency steroids. Warn pt that it will take a long time
to go away
Erythema Nodosum
Inflammatory eruption of subcutaneous fat (panniculitis)
Tends to affect the shins
Poorly demarcated warm erythematous nodules
Multiple etiologies –NODOSUM
NO- no obvious cause (idiopathic) most common
D- drugs sulfonamides, ocp, penicillin, vaccines, bromide
O- oral contraceptive pill, pregnancy
S- sarcoidosis
U- ulcerative colitis (IBS), Behcet Disease
M- microbiology
Bacterial – strep, campy, yersinia, TB, leprosy
Fungal- Blastomycosis, coccidiomycosis, histoplasmosis
Viral- HSV, Mono
Parasites- Leishmaniasis, toxoplasmosis
Management: CBC, blood cultures, throat swab if symptomatic, urine HCG, CXR for
sarcoid. Should resolve on own.