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Dermatologic Emergencies PowerPoint Presentation

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Description : Check out this medical presentation on Staphylococcal Scalded Skin Syndrome, which is titled "Dermatologic Emergencies", to know about the clinical clues to the diagnosis of potentially life-threatening dermatologic conditions, describe the clinical presentation of important dermatologic emergencies, and know the infectious and pharmacologic causes of life-threatening dermatoses.

Tags : Staphylococcal Scalded Skin Syndrome, Dermatologic Emergencies, dermatologic conditions

Published on : Jul 05, 2021 | Views : 3506 | Downloads : 9

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Slide 1-

Dermatologic Emergencies Amy Y-Y Chen, MD, FAAD amychen@bu.edu Boston University School of Medicine Internal Medicine Noon Conference
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Conflicts of Interests No Conflicts of Interests
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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
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Outline Introduction Infections Bacterial Viral Life threatening drug eruptions Others
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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
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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”
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Inpatient Consults CLEAR AND DEFINED question
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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
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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
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Infections Bacterial Viral
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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
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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
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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
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Staphylococcal Scalded Skin Syndrome
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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
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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
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Necrotizing fasciitis
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Necrotizing fasciitis Clinical presentation Shock and organ failure Management Also need surgical debridement of the necrotic tissue
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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
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Meningococcemia Clinical presentation Flu like symptoms: fever, chills, malaise DIC, shock, death
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Meningococcemia
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Rocky Mountain Spotted Fever Etiology Rickettsia Rickettsii carried by ticks Only 60% aware of tick bites Geographic location
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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
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Rocky Mountain Spotted Fever First starts on wrists and ankles
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Rocky Mountain Spotted Fever
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Rocky Mountain Spotted Fever
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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
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Infections Bacterial Viral
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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
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Eczema Herpeticum
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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
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Varicella Infection
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Varicella Infection Dermatologic findings Zoster Follows dermatome distribution
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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
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Management Treatment of underlying infections Antibiotics, broad spectrum until organism identified Antiviral Supportive care with fluid and electrolyte management
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Life Threatening Drug Eruptions
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Life Threatening Drug Eruptions Risk factors: HIV or immunosuppressed patients Elderly (polypharmacy) Genetic predisposition Management Stop the medication Supportive care
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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%
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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
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SJS/TEN
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SJS/TEN
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SJS/TEN Management Burn unit, ICU Ophthalmology, urology IVIG Systemic steroid is controversial
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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
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DRESS Dermatologic findings Maculopapular (morbilliform) and urticarial eruption most common Vesicles, bullae, pustules, purpura, targetoid lesions, erythroderma Facial edema (mistaken for angioedema)
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DRESS Clinical presentation Fever, eosinophilia, lymphadenopathy, Hepatic damage (can be fulminant), endocrinopathy, myocarditis Management Systemic corticosteroid with slow taper
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Others
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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
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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
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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)
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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
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Erythroderma
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Erythroderma Management Supportive care with fluid and electrolyte Need to search for underlying causes-> treatment of underlying dermatoses (topical corticosteroids, emollients) Abx of signs of infection Mortality is 18%
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Question 1: This patient presents with few days history of malaise and decrease oral intake. What is the most appropriate therapy? Topical antibiotics Oral antibiotics IV antiviral Topical antiviral Topical steroids
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Question 2: This patient was given sulfonamides two weeks ago for an UTI. She now presents to the ED with painful skin, which one of the following is the most important first step? Start IVIG NSAID for pain control Start high dose systemic steroids Stop the sulfonamides Call dermatology
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Question 3: The patient in Question 2 is now stabilized and in the Burn unit. What organ system(s) can potentially be involved in the disease process? Eyes Aerodiguestive track Urinary tract All of the above None of the above
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Question 1: This patient presents with few days history of malaise and decrease oral intake. What is the most appropriate therapy? Topical antibiotics Oral antibiotics IV antiviral Topical antiviral Topical steroids
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Question 2: This patient was given sulfonamides two weeks ago for an UTI. She now presents to the ED with painful skin, which one of the following is the most important first step? Start IVIG NSAID for pain control Start high dose systemic steroids Stop the sulfonamides Call dermatology
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Question 3: The patient in Question 2 is now stabilized and in the Burn unit. What organ system(s) can potentially be involved in the disease process? Eyes Aerodiguestive track Urinary tract All of the above None of the above
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Selected Future Reading Usatine RP and Sandy N. Dermatologic Emergencies. Am Fam Physician. 2010; 82: (7): 773-780 Kress DW. Pediatric dermatology emergencies. Current Opinion in Pediatrics. 2011; 23:403-406. Freiman A, Borsuk D and Sasseville D. Dermatologic emergencies. CMAJ. 2005; 173 (11): 1317-1319. OR you can rotate with us !! References (including images) Dermatology Fitzpatrick’s Dermatology Fitzpatrick’s color atlas and synopsis of clinical dermatology DermNet.NZ eMedicine
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THANK YOU FOR YOUR ATTENTION ! amychen@bu.edu