Things that make you go ughhh…. Adult Dermatology Heather Patterson PGY-2 Feb 22, 2007

Things that make you go ughhh…. Adult DermatologyHeather Patterson PGY-2

Feb 22, 2007

Objectives • Learn key features of toxic rashes seen in

adults.

• Win the container of homemade chocolate chip cookies!

• Small solid elevation <1cm

Describe:

PAPULE

Describe:

• Palpable mass > 1cm NODULE

Describe:

• Elevated disc shaped lesion

PLAQUE

Describe:

• Flat area of discolouration

MACULE

Describe:

• Fluid filled area <0.5cmVESSICLE

Describe:

• Fluid filled area >0.5cmBULLAE

Describe:

• Area of dermal edema, raised, erythematousURTICARIA

Describe:

• Denuded area where epidermis is lost EROSION

Describe:

• Denuded area where dermis is lost

ULCER

Describe the rash.

Rocky Mountain Spotted Fever

Etiology?• Rickettsia rickettsee – found in Rocky Mountain wood tick saliva

How many hours does the tick need to feed for innoculation?

• 6 hours

Rocky Mountain Spotted Fever

• Clinical Presentation– Day 2-14 after bite– Sudden onset fever (>38.3) and rigors– Nausea/vomiting, anorexia– Headache, myalgias – Rash

Rocky Mountain Spotted Fever

How does the rash present on day 2-4 post onset fever?

• 2-6 mm blanchable pink macules starting on wrists and ankles

• Spreads cetripetally and includes palms and soles

Rocky Mountain Spotted Fever

How does the rash present on day 5-6 post onset fever?

• Non-blanchable petechial rash• Local edema surrounding petechie

Rocky Mountain Spotted Fever

• Labs:– Bands– Thrombocytopenia– ↑Na– ↑ Transaminases

Rocky Mountain Spotted Fever

• Doxycycline– 100mg po bid – 2.2 mg/kg for kids

• Chloramphenicol– In pregnancy

Treatment? Duration?

• Treat for 3 days after afebrile OR min of 5-7 days

Rocky Mountain Spotted Fever

• Mortality:– Untreated >30%– Treated 3-7%

Describe the rash.

Meningococcemia

• Clinical Presentation– Myalgias, malaise, sudden onset fever– +/- signs of meningitis– Rash

• Etiology– N. meningitidis– Droplet spread

Meningococcemia

How does the rash present early?

• Non specific erythematous lesions that look viral

Meningococcemia Classic appearance?

• Irregular borders, small• Pupura are painful and slightly raised• Usually on trunk and ext. but can be

anywhere

Meningococcemia

• Ceftriaxone and Vanco until isolated• Pen G 250 000U/kg/day divided q12h

Treatment?

Prophylaxis?• Rifampin 600mg q12h (5-10 mg/kg)

• Cipro 500mg IM x1• Ceftriaxone 250mg IM x1 (125mg for

kids)

Meningococcemia

• 40%

What is the mortality with this rash?

Describe the rash.

EM

Classic Rash?

• Target lesions• Progression: Macules Papules Central

Vessicles

EM - distribution

EMMucous membrane

involvement?

• EM – Minor: little to none• EM Major: always

Erythema Multiforme

• Drugs• Infection

– Herpes simplex– Mycoplasma

• Idiopathic (>50%)

Etiology?

Erythema Multiforme • Pathophysiology

– Perivascular mononuclear infiltrate– Dermal edema– Secondary epidermal changes

EM • EM Minor:

– Classic target lesions usually on face and extremities

– Vessicles but no bullae– Little to no MM involvement– Recurrent episodes associated with Herpes

simplex

EM • EM Major

– Target lesions more generalized– Bullae and + Nicholsky sign– Extensive MM involvement and systemic features:

• Conjunctivitis/corneal ulcers, uveitis• Cheilitis, stomatitis, GI erosions, resp tract erosions• Vulvitis, balanitis

– May progress to SJS/TEN – Most often a drug reaction

Describe the rash.

SJS/TEN Name 3 causes of

this rash.• Drugs, infection (mycoplasma, viral), vaccination, chemicals

Name 3 drug /classes that can cause this rash.• Sulfa

• Anticonvulsants• NSAIDs – oxicams• Allopurinol

SJS/TEN

• Pathophysiology– Cytotoxic immune reaction against

keratinocytes– Leads to vasculitis of superficial dermis and

epidermal necrosis

SJS/TEN

• Most consider this a spectrum of disease:– EM major SJS TEN

• May start with classic target lesions of EM BUT

about 50% of SJS/TEN do not have target lesions

SJS/TEN What %BSA is

involved in SJS?• <10%

What %BSA is involved in TEN

• >30%

SJS/TEN • Clinical Presentation

– Onset within 1-3 weeks of first exposure to antigen (repeat exposure has faster onset, ie days)– 2-3 day prodrome prior to rash:

• Cough, sore throat• Myalgias, malaise, headache• Anorexia• Fever• Skin burning, itching, tenderness• Conjunctival burning, itchiness

SJS/TEN

Prodromal Rash?

• PAINFUL, WARM• Mobilliform with diffuse erythema

SJS/TEN

How does the rash present early?

• Discrete dark red macules with crinkled surface

• Enlarge and eventually coalesce

SJS/TEN

How does the rash appear late?

• Raised FLACCID blisters• Confluent and necrotic with epidermis

sloughing in sheets leaving red dermis exposed

SJS/TEN

What is Nicholsky’s sign?

• Firm sliding pressure causes blistering/sloughing of normal appearing skin.

SJS/TEN

Mucous membrane involvement?

• Yes in 92-100% of cases• 85% have conjunctival lesions

SJS/TEN • Other findings/complications:

– Fever >38– Heme:

• Anemia• Neutropenia (coreltates with poor prognosis)

– GI, Resp• Epithelial erosions

– Renal• ATN, ARF

– Sepsis

SJS/TEN

• Supportive• Clean saline soaked gauze bandages• Avoid silver sulfadiazine• Fluids

– fluid replacement required for 3 degree thermal burn of similar BSA

Treatment in ED?

SJS/TEN

• High dose steroids• Cyclosporin/cyclophosphamide• Plasmaphoresis/IVIG• NAC• Erythromycin for eye involvement

Treatment outside ED?

SJS/TEN

• SJS – 5%• TEN – 30%

Mortality?

Describe the rash.

Staph Scalded Skin Syndrome

• Clinical Presentation– Seen in kids AND immunocompromised, alcholics,

CRF, malignancy– Often have primary infection– Fever, malaise– Skin tenderness in flexural areas prior to sloughing

• Pathophysiology– Staph exfoliative toxin targets zona granulosa– Causes intraepidermal splitting leading to

bullae formation

SSSS

How does the rash present early?

• Macular sandpaper rash with erythema• Deeper coloured erythema with skin

tenderness in flexural areas

SSSS

How does the rash present 24-48h post pain?

• FLACCID bullae in erythem regions

• Bullae coalesce and rupture leaving erythem base

• Looks like wet tissue paper

• Palms, soles, MM spared

SSSS Positive Nicholsky’s

sign?MM involvement?

• Yes BUT only on erythematous skin• No MM involvement or very mild

inflammation

SSSS

• Supportive• Clean saline soaked gauze bandages• May require ABx

– Clox– 1st gen cephalosporin– Vanco for MRSA– Macrolide

Treatment in ED?

SSSS

• Kids – 3%• Healthy adults – up to 50%• Adults with comorbidities – up to 100%

Mortality ?

Describe the rash.

Staph TSS Classic appearance?

• Fine erythematous macular sandpaper rash – looks like scarlet fever

• Extensive generalized non pitting edema• +MM involvement

Staph TSS What is the most common

underlying cause of this rash?• Tampons Name 2 other

causes.• Surgical wounds with abscess• Burns• Ulcers• Insect bites• Contraceptive devices

Staph TSS • Pathophysiology

– Production of endotoxin during bacterial replication

– Act as superantigen to T cells leading to massive cytokine release

Staph TSS – diagnostic criteria

1. Fever ≥ 38.92. Rash3. Hypotension or orthostatic hypotension4. Involvement of 3 of the following

1. GI – vomiting and diarrhea2. Muscular – severe myalgias or CK 2x normal3. MM involvement4. Renal – Cr or BUN 2x normal or pyuria5. Hepatic – bili, transaminases 2x normal6. CNS – confusion, headache, seizure, no focality7. Heme – thrombocytopenia plts < 100

Staph TSS – diagnostic criteria

5. Desquamation 1-2 weeks post onset illness6. Evidence against alternative diagnosis

Staph TSS

• ABCs• May require – pressors/ionotropes• ++ Fluid resuscitation• ABx

– Cloxacillin, naficillin – Clinda – Vanco if MRSA

• Find and treat source– Remove tampon, drain abscess etc

Treatment in ED?

Describe the rash.

Pemphigus Vulgaris • Pathophysiology

– Autoimmune disease– Loss of cell to cell adhesion in the epidermis

due to antibody binding to surface glycoproteins

Pemphigus Vulgaris

• Presentation:– Oral and MM involvement – painful bullae with

ulceration– May complain of epistaxis, hoarseness,

dysphagia, wt loss– Gums and vermillion boarders are common

locations

– Cutaneous lesions– General malaise

Pemphigus Vulgaris

Mucosal Lesions?

• Fragile bullous lesions • Become non healing painful ulcers

Pemphigus Vulgaris

Classic Appearance?

• FLACCID fragile bullae found on normal looking skin in a random pattern– But commonly seen on face,

scalp and upper trunk• Become non healing

painful ulcers

Pemphigus Vulgaris

Nicholsky sign?

• Positive

Pemphigus Vulgaris

• Supportive, analgesia, wound care• Prednisone 2-3mg/kg/day

– Treat until no new blisters are forming AND negative Nicholsky sign

• Consult Dermatology

Treatment in ED?

• Immune modulators– Derm

Describe the rash.

Bullous Pemphigoid

• Epidemiology– Most often seen in the elderly and men

• Pathophysiology– Most common autoimmune blistering disease– Antibody to basement membrane leads to

complement deposition and subepidermal blister formation

Bullous Pemphigoid

Classic Appearance?• TENSE bullae with

preference for:– Lower abdo, inner thighs,

groin, flexor surfaces of extrem.

• On normal or erythematous skin

• 66% with erythem or urticarial lesions prior to bullae

• Severe pruritis

Bullous Pemphigoid

Nicholsky sign?

• Negative

Pemphigoid • MM involvment?

– In 30% of patients

Pemphigoid

• Supportive• Wound care• Prednisone 0.5mg/kg/day

AND Clobetasone proprionate 40g/d divided bid

(or other high potency topical steriod)

• Consult Dermatology

Treatment in ED?

Bullous Pemphigoid

Mortality?

• 25-40% – Most common causes: secondary sepsis or

physiological stress leading to MI

Varicella Zoster What is Hutchison’s

sign?• Involvement of the nasociliary nerve – lesions on the tip of the nose.

What is the concern with this distribution?• Involvement of the eye

• Conjunctivitis, Corneal inflammation and scarring

• Uveitis, iritis

Varicella Zoster Ophthalmicus

• Acyclovir 800mg 5x daily x7-10daysOR

• Famciclovir 500mg tid x 7days• Consider IV if severe

• Referral to ophtho within 24h

Treatment in ED?

Conclusion • Hopefully you have learned key features

of several emergent rashes seen in adults!