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Dermatologic Emergencies

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

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  1. Dermatologic Emergencies Boston University School of Medicine Internal Medicine Noon Conference July 26th 2013 Amy Y-Y Chen, MD, FAAD amychen@bu.edu

  2. Conflicts of Interests • No Conflicts of Interests

  3. 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

  4. Outline • Introduction • Infections • Bacterial • Viral • Life threatening drug eruptions • Others

  5. 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

  6. 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”

  7. Inpatient Consults CLEAR AND DEFINED question

  8. 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

  9. 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

  10. Infections Bacterial Viral

  11. 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

  12. 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

  13. 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

  14. Staphylococcal Scalded Skin Syndrome

  15. 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

  16. 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

  17. Necrotizing fasciitis

  18. Necrotizing fasciitis • Clinical presentation • Shock and organ failure • Management • Also need surgical debridement of the necrotic tissue

  19. 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

  20. Meningococcemia • Clinical presentation • Flu like symptoms: fever, chills, malaise • DIC, shock, death

  21. Meningococcemia

  22. Rocky Mountain Spotted Fever • Etiology • Rickettsia Rickettsii carried by ticks • Only 60% aware of tick bites • Geographic location

  23. 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

  24. Rocky Mountain Spotted Fever First starts on wrists and ankles

  25. Rocky Mountain Spotted Fever

  26. Rocky Mountain Spotted Fever

  27. 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

  28. Infections Bacterial Viral

  29. 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

  30. Eczema Herpeticum

  31. 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

  32. Varicella Infection

  33. Varicella Infection • Dermatologic findings • Zoster • Follows dermatome distribution

  34. 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

  35. Management • Treatment of underlying infections • Antibiotics, broad spectrum until organism identified • Antiviral • Supportive care with fluid and electrolyte management

  36. Life Threatening Drug Eruptions

  37. Life Threatening Drug Eruptions • Risk factors: • HIV or immunosuppressed patients • Elderly (polypharmacy) • Genetic predisposition • Management • Stop the medication • Supportive care

  38. 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%

  39. 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

  40. SJS/TEN

  41. SJS/TEN

  42. SJS/TEN • Management • Burn unit, ICU • Ophthalmology, urology • IVIG • Systemic steroid is controversial

  43. 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

  44. DRESS • Dermatologic findings • Maculopapular (morbilliform) and urticarial eruption most common • Vesicles, bullae, pustules, purpura, targetoid lesions, erythroderma • Facial edema (mistaken for angioedema)

  45. DRESS • Clinical presentation • Fever, eosinophilia, lymphadenopathy, • Hepatic damage (can be fulminant), endocrinopathy, myocarditis • Management • Systemic corticosteroid with slow taper

  46. Others

  47. 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

  48. 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

  49. 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)

  50. 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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