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11/7/2017 Goals of this talk HospitalBased Dermatology: Common and Tough Consult Cases Present common morphologies that arise during inpatient consultations Lindy P. Fox MD Associate Professor of Clinical Dermatology Director,


  1. 11/7/2017 Goals of this talk Hospital‐Based Dermatology: Common and Tough Consult Cases • Present common morphologies that arise during inpatient consultations Lindy P. Fox MD Associate Professor of Clinical Dermatology Director, Hospital Consultation Service • Generate a working differential diagnosis University of California, San Francisco lindy.fox@ucsf.edu • Use cases to demonstrate key teaching points about diagnosis or management I have no relevant conflicts of interest to disclose. I may discuss off‐label uses of medications . Common Morphologies in the Hospital Morbilliform • Measles‐ like 1. Morbilliform • Pink to red macules and papules 2. Cellulitic plaques – No surface change 3. Purpura • May be called “maculopapular” 4. Ulcers • Most common differential in the hospital: 5. Vesiculobullous – Drug eruption – Viral exanthem 6. Pustules – Acute Graft vs. Host Disease • Most often doesn’t need a biopsy 1

  2. 11/7/2017 Drug Eruptions: Drug Induced Hypersensitivity Syndrome Degrees of Severity • Skin eruption associated with systemic symptoms and alteration of internal organ function Simple Complex • “ DRESS ” ‐ Drug reaction w/ eosinophilia and systemic symptoms Morbilliform drug eruption Drug hypersensitivity reaction Stevens-Johnson syndrome • “ DIHS ” = Drug induced hypersensitivity syndrome (SJS) • Begins 2‐ 6 weeks after medication started Toxic epidermal necrolysis – time to abnormally metabolize the medication (TEN) • Role for viral reactivation, esp HHV6, CMV, EBV Minimal systemic symptoms – Can check these PCRs Systemic involvement • Mortality 10% Potentially life threatening DIHS‐ Clinical Features DIHS‐ Drugs • Rash • Aromatic anticonvulsants – FACIAL EDEMA • Fever (precedes eruption by day or more) – phenobarbital, carbamazepine, phenytoin • Pharyngitis – THESE CROSS‐REACT • Hepatitis • Sulfonamides • Arthralgias • Lamotrigine • Lymphadenopathy • Dapsone • Hematologic abnormalities • Allopurinol (HLA‐B*5801) – eosinophilia – atypical lymphocytosis • NSAIDs • Other organs involved • Other – Interstitial pneumonitis, interstitial nephritis, thyroiditis – Abacavir (HLA‐ B*5701) – Myocarditis‐ acute eosinophilic mycocarditis or acute necrotizing – Nevirapine (HLA‐DRB1*0101) eosinophilic myocarditis • EKG, echocardiogram, cardiac enzymes – Minocycline, metronidazole, azathioprine, gold salts 2

  3. 11/7/2017 Drug Induced Hypersensitivity Syndrome DIHS‐ Treatment • Stop the medication • Each class of drug causes a slightly different clinical picture • Follow CBC with diff, LFT ’ s, BUN/Cr • Facial edema characteristic of all • Avoid cross reacting medications!!!! • Anticonvulsants: – Aromatic anticonvulsants cross react (70%) – 3 weeks • Phenobarbital, Phenytoin, Carbamazepine – Atypical lymphocytosis, hepatic failure • Valproic acid and levetiracetam (Keppra) generally safe • Dapsone: • Systemic steroids (Prednisone 1.5‐2mg/kg) – 6 weeks – Taper slowly‐ 1‐3 months – No eosinophilia • For allopurinol start steroid sparing agent • Allopurinol: (mycophenolate mofetil) – 7 weeks • Completely recover, IF the hepatitis resolves – Elderly patient on thiazide diuretic • Check TSH monthly for 6 months – Renal failure • Watch for late cardiac involvement – Requires steroid sparing agent to treat (avoid azathioprine) – Counsel patient Cellulitic Plaques Cellulitis • Infection of the dermis • Red, edematous plaques • Gp A beta hemolytic • Often warm, tender strep and Staph aureus • If itchy, think contact dermatitis • Rapidly spreading • Most common differential in the hospital: • Erythematous, tender – Cellulitis plaque, not fluctuant – Stasis dermatitis • Patient often toxic – Contact dermatitis • WBC, LAD, streaking • Don’t miss – Pyomyositis • Rarely bilateral • Rarely needs a biopsy • Treat tinea pedis • Bacterial culture any open or draining area • If bilateral, think stasis dermatitis, contact dermatitis 3

  4. 11/7/2017 Stasis Dermatitis Called to evaluate cellulitis not responding to vancomycin • Often bilateral, L>R • Itchy and/or painful • Red, hot, swollen leg Exquisite pain +/‐Persistent • No fever, elevated WBC, fever LAD, streaking Not responding • Look for: varicosities, to antibiotics edema, venous ulceration, No LAD hemosiderin deposition • Superimposed contact dermatitis common Question: Question: Your Next Step Is: Your Next Step Is: 1. ID consult 1. ID consult 2. MRI 2. MRI 3. Ultrasound 3. Ultrasound 4. Surgery consult 4. Surgery consult 5. Add gram negative coverage 5. Add gram negative coverage 4

  5. 11/7/2017 Pyomyositis • Acute primary bacterial infection of skeletal muscle  “ Bag of pus ” • Trauma, travel, immunosuppression, diabetes • Etiologic Agents – Staphylococcus aureus (77%) – Streptococcus species (12%) • Group A streptococcus • Not helpful: fever, CK, labs, blood cultures • Image: MRI > CT > US • Treatment: surgical drainage + antibiotics Palpable purpura • Nonblanching red to purple papules • Most common differential in the hospital: – Small or mixed (small and medium) vessel vasculitis – Secondary hemorrhage into papular process • Always needs a biopsy for H+E, direct immunofluorescence, culture • Consult dermatology if possible 5

  6. 11/7/2017 Consult: 23F, 2 weeks of palpable purpura, calf pain, arthralgias, and abdominal pain Vasculitis • Clinical morphology correlates with the size of the affected vessel – Small vessel disease (post capillary venules) • Urticaria and palpable purpura – Small‐artery disease • Subcutaneous nodules – Medium‐vessel disease • Organ damage, livedo, purpura, mononeuritis multiplex – Large‐vessel disease • Claudication and necrosis 6

  7. 11/7/2017 Palpable Purpura‐ Leukocytoclastic Vasculitis Palpable Purpura • Conditions associated with LCV • Immune complex vasculitis • Pauci‐immune complex – Idiopathic (45‐55%) – Idiopathic, infection, drug, vasculitis – Infection (15‐20%) malignancy – ANCA‐ associated – IgA vasculitis, Henoch‐Schönlein • Microscopic polyangiitis – Inflammatory diseases (15‐20%) purpura • Granulomatosis with – Urticarial vasculitis polyangiitis – Medications (10‐15%) • Eosinophilic granulomatosis – Hypergammaglobulinemic – Malignancy (<5%) with polyangiitis purpura of Waldenström – Levamisole – Bowel‐bypass syndrome – Sweet ’ s syndrome – Mixed cryoglobulinemia – Connective tissue disease associated Palpable Purpura “ PLUS ” Small Vessel Vasculitis‐ Evaluation • • H+P, including medications – Blood culture Size of vessels is a clinical clue to underlying etiology – CBC with differential and ROS • Medium‐sized vessel involvement leads to • Skin biopsy for H+E, direct – Urinalysis with micro dermal/subcutaneous nodules, ulcerations, livedo, – Creatinine immunofluorescence, and/or retiform purpura – Stool guaiac culture • Differential diagnosis – Rheumatoid factor • – ASO, throat culture IgA vasculitis – Hepatitis B, C serologies • Septic vasculitis – ANA • ANCA‐associated vasculitis – Complement • Levamisole – ANCA • Mixed cryoglobulinemia – Cryoglobulins • Connective tissue disease associated – Immunofixation electrophoresis • Leukemic vasculitis – PPD or quantiferon gold • Polyarteritis nodosa (very rare) – Toxicology screen (levamisole) • More than one process occurring simultaneously – Age appropriate malignancy screen 7

  8. 11/7/2017 Ulcers Case • 67M ‐elective saphenous vein phlebectomy • Breakdown of skin to reveal dermis • 4d post op ‐erythema around wound • Multiple debridements and broad spectrum • Most common differential in the hospital: antibiotics – Venous insufficiency ulcers • Ulcer continues to expand – Pyoderma gangrenosum – Viral infections (HSV, CMV) • Wound cultures are negative • Tmax 104, WBC 22 • Culture for bacteria and virus when suspect • Transferred to UCSF 3 weeks later infection • Biopsy may be helpful – Send for H+E and culture Pyoderma Gangrenosum Pyoderma Gangrenosum • Rapidly progressive (days) ulcerative process • 50% have no underlying cause • Begins as small pustule which breaks down forming • Associations (50%): an ulcer • Undermined violaceous border – Inflammatory bowel disease (1.5%‐5% of IBD • Expands by small peripheral satellite ulcerations patients get PG) which merge with the central larger ulcer – Rheumatoid arthritis • Occur anywhere on body – Seronegative arthritis • Triggered by trauma (pathergy) – Hematologic – surgical debridement, attempts to graft abnormalities (AML) 8

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