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Dermatologic Emergencies. Boston University School of Medicine Internal Medicine Noon Conference July 26th 2013. Amy Y-Y Chen, MD, FAAD amychen@bu.edu. Conflicts of Interests. No Conflicts of Interests. Objectives.
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Dermatologic Emergencies Boston University School of Medicine Internal Medicine Noon Conference July 26th 2013 Amy Y-Y Chen, MD, FAAD amychen@bu.edu
Conflicts of Interests • No Conflicts of Interests
Objectives • Identify clinical clues to the diagnosis of potentially life-threatening dermatologic conditions • Describe the clinical presentation of important dermatologic emergencies • Discuss infectious and pharmacologic causes of life-threatening dermatoses
Outline • Introduction • Infections • Bacterial • Viral • Life threatening drug eruptions • Others
Introduction • ~15-20 % of visits to primary care physicians and emergency departments are due to dermatologic complaints • It is important to be differentiate simple skin conditions from the more serious, life threatening conditions that require immediate intervention
Clues to the Presence of a Potential Dermatologic Emergency Fever and rash Fever and blisters or denuding skin Rash in immunocompromised Palpable purpura “Full body redness”
Inpatient Consults CLEAR AND DEFINED question
Inpatient Consults • Have seen and examined the patient and able to provide some pertinent hx • Not acceptable: • “Saw a derm note in EMR” • “Something on the skin” • “Patient being discharged today, needs stat consult” • MD to MD contact • If patient has pre-existing derm problem and was doing well on therapy, consider keeping them on therapy when they are admitted
Inpatient Consults • Benefits and limitation of biopsy • Not black and white • Takes a few days to come back • Tissue cultures can take a few weeks • Suture removal • Follow up on recommendation • Topical therapy takes a few days to a week to work
Infections Bacterial Viral
Staphylococcal Scalded Skin Syndrome • Etiology • Toxin-mediated cleavage of the skin at granular layer resulting in a split • Risk factors: newborn, children or adults w/ renal failure
Staphylococcal Scalded Skin Syndrome Dermatologic findings Erythema periorificially on the face, neck, axilla, groin. Then generalized within 48 hrs as the color deepens Skin tenderness Flaccid bullae w positive Nikolsky sign Within 1-2 days, flexural areas begin to slough off Complete re-epithelialization in 2 weeks
Nikolsky Sign • Positive when a blister occurs on normal appearing skin after application of lateral pressure w/ a finger • Occurs in any superficial blistering process
Staphylococcal Scalded Skin Syndrome • Clinical presentation • Prodrome of fever, malaise, sore throat • Complication • Mortality rate is 3% in kids, > 50% in adults and 100% in adults with underlying diseases • If in newborn nursery, needs isolation • Identify possible staph carrier
Necrotizing fasciitis • Etiology • Necrosis of subcutaneous tissue due to infection • Type I : mixed anaerobes, gram negative aerobic bacilli and enterococci • Type II: group A streptococci • Risk factors: diabetes, peripheral vascular disease, immunosuppression • Dermatologic findings • Diffuse edema and erythema of the affected skin-> bullae-> burgundy color-> gangrene • Severe pain, anesthesia. crepitus, exudates
Necrotizing fasciitis • Clinical presentation • Shock and organ failure • Management • Also need surgical debridement of the necrotic tissue
Meningococcemia • Etiology • Neisseria meningitides (gram neg diplococcus) spread by respiratory route • Often seen in young adults and children • Risk factor: asplenia, immunoglobulin or terminal complement deficiencies • Dermatologic findings • Abrupt onset of maculopapular or petechial eruption on acral surface, trunk or lower extremities -> progression to purpura in hours • Angular edge with “gun metal gray” center • +/- mucosal involvement
Meningococcemia • Clinical presentation • Flu like symptoms: fever, chills, malaise • DIC, shock, death
Rocky Mountain Spotted Fever • Etiology • Rickettsia Rickettsii carried by ticks • Only 60% aware of tick bites • Geographic location
Rocky Mountain Spotted Fever Dermatologic findings Purpuric macules and papules Starts on the wrists and ankles within 2 weeks-> spread to palms, soles-> to trunk and face Over 2-4 days, the skin will become hemorrhagic and petechial May have eschar at site of bite
Rocky Mountain Spotted Fever First starts on wrists and ankles
Rocky Mountain Spotted Fever • Clinical presentation • Triad: fever, headache and rash (only in 60%) • Can have variety of organ involvement (cardiogenic shock, hepatic failure, renal failure, meningismus and DIC) • Management • Mortality is 30-70% if untreated vs 3-7% if treated • Ideally should start within 5 days of infection • DOXYCYCLINE ! Even in kids
Infections Bacterial Viral
Eczema Herpeticum • Kaposi’s varicelliform eruption • Etiology • Herpes virus: HSV1 > HSV2 • Risk factor: any diseases w impaired skin barrier • Dermatologic findings • 2-3 mm umbilicated vesicles-> punched out erosions-> hemorrhagic crusts • If severe, may have systemic involvement
Varicella Infection • Etiology • Varicella Zoster Virus (VZV or HSV3) • Causes of chicken pox (primary infection) and shingles (reactivation) • Dermatologic findings • Primary • Pruiritic erythematus macules and papules-> vesicles with clear fluid surrounded by narrow red halos (dew drops on a rose petal) • Lesions in all stages of development
Varicella Infection • Dermatologic findings • Zoster • Follows dermatome distribution
Varicella Infection Zoster Prodrome in 90% Disseminated lesions (> 20 vesicles outside of the area of primary or adjacent dermatomes) and/or visceral involvement seen in approximately 10% of immunocompromised patients V1 Distribution
Management • Treatment of underlying infections • Antibiotics, broad spectrum until organism identified • Antiviral • Supportive care with fluid and electrolyte management
Life Threatening Drug Eruptions • Risk factors: • HIV or immunosuppressed patients • Elderly (polypharmacy) • Genetic predisposition • Management • Stop the medication • Supportive care
Stevens-Johnson Syndrome (SJS)/Toxic Epidermal Necrolysis (TEN) • Pathophysiology: • Drug induced mucocutaneous reaction • Culprit medications: Sulfonamides, anticonvulsants, allopurinol, NSAIDs. Usually given 1-3 weeks before onset • Genetic susceptibility • SJS and TEN are continuum • SJS: BSA < 10% • SJS/TEN overlap: BSA 10-30% • TEN: BSA > 30%
SJS/TEN • +/- Clinical presentation • Prodrome: fever, chills, malaise • Stinging eyes, difficulty swallowing and urinating • Dermatologic findings • Skin tenderness • Dusky erythema • Epidermal detachment and desquamation • Mucosal involvement
SJS/TEN • Management • Burn unit, ICU • Ophthalmology, urology • IVIG • Systemic steroid is controversial
DRESS • DRESS: Drug Reaction with Eosinophilia and Systemic Symptoms • Anticonvulsant hypersensitivity syndrome • Drug-induced hypersensitivity syndrome • Hypersensitivity syndrome • Drug-induced delayed multi-organ hypersensitivity syndrome • Pathophysiology: • Idiosyncratic, problem with drug detoxification • Drug exposure to onset of symptoms 2-6 wks • Common culprit: aromatic anticonvulsant, sulfonamides, minocycline, allopurinol, antiretroviral drugs, NSAIDS, CCB
DRESS • Dermatologic findings • Maculopapular (morbilliform) and urticarial eruption most common • Vesicles, bullae, pustules, purpura, targetoid lesions, erythroderma • Facial edema (mistaken for angioedema)
DRESS • Clinical presentation • Fever, eosinophilia, lymphadenopathy, • Hepatic damage (can be fulminant), endocrinopathy, myocarditis • Management • Systemic corticosteroid with slow taper
Angioedema • Pathophysiology • Increased intravascular permeability • Dermatologic findings • Well circumscribed acute cutaneous edema due to increased intravascular permeability • Face, lips, extremities, genitalia • Painful, usually not pruritic • Clinical presentation • Abdominal pain • Respiratory distress
Angioedema • Etiology: • Often idiopathic • Medications • angiotensin-converting- enzyme inhibitor in 10-25% of cases • Penicillin • NSAID • Allergens (foods, radiographic contrast media) • Physical agents (cold, vibration, etc) • C1 esterase inhibitor deficiency: hereditary vs associated with autoimmune disorder or malignancy
Angioedema • Management • Airway management • Antihistamines • Cool compresses • Avoid triggers • For pts with C1 esterase inhibitor deficiency: • Acute management vs short term vs long term prophylaxis: androgens (danazol and stanozolol), C1 esterase inhibitor concentrate, antifibrinolytics, icatibant (selective antagoist of bradykinin B2 receptor)
Erythroderma • Dermatologic findings • Generalized erythema involving 90% of BSA • Pruritus • Clinical presentation • Fever, malaise • Excessive vasodilatation-> protein and fluid loss • Hypotension, electrolyte imbalance, congestive heart failure • Etiology: • 50% due to preexisting dermatoses • Seborrheic dermatitis, contact dermatitis, lymphoma (CTCL), leukemia, atopic dermatitis, psoriasis, pityriasis rubra pilaris, idiopathic, drugs (esp in HIV pts) • Search for clues on physical examination