Why this lecture? Rashes to recognize in ER. Conflict of interest none. Objectives 11/15/17. Contest is the key!

Transcription

1 Rashes to recognize in ER Peter Tzakas, MD MBChB CCFP Nino Parunashvili, PA student Conflict of interest none Objectives Anatomy and basic dermatological term review Recognize common dermatological conditions Recognize dangerous dermatological conditions Know diagnostic and treatment options for those conditions Have some fun Why this lecture Contest is the key! 1

2 Anatomy Skin functions Protection: barrier to UV radiation, mechanical and chemical insults, pathogens, and dehydration Thermal: insulation to maintain body temp in cold and dissipation of heat in warm environments Sensation: largest sensory organ of the body-> touch, pain, temperature Metabolic: Vit D synthesis, energy storage (primarily in form of TG) Definitions Profile < 1 cm diameter > 1 cm diameter Flat lesion Macule (e.g. freckle) Patch (e.g. vitiligo) Raised superficial lesion Papule (e.g. wart) Plaque (e.g. psoriasis) Deep palpable Nodule (e.g. dermatofibroma) Tumour (e.g. lipoma) Elevated fluid filled lesion Vesicle (e.g. HSV) Bulla (e.g. bullous pemphigoid) Medical History question When did the rash start How did it start, evolve Distribution (MM, palms, soles, etc) What makes it better/ what makes it worse Associated symptoms: itch, fever, viral symptoms Is this first time you are having such a rash Changes in diet, environment Sick contacts, Travel history PMH, Meds, Allergies Family history DDx to consider Tintinalli s Emergency Medicine 1. Cellulitis Acute, painful, spreading infection of dermis and subcutaneous tissue Pathogens: S. aureus, Strep. Pyogenes... 1 st line: Cefazolin/ cephalexin or cloxacillin 2 nd line: erythromycin or clindamycin Children: cefuroxime Diabetics: TMP/ SMX and metronidazole 2

3 Description 2. Impetigo A superficial skin infection, highly contagious Honey colored crusting, weeping, oozing of the skin Pathogens: S. aureus, Strep. Pyogenes Mild disease: topical agents (Bacitracin, Mupirocin) Severe disease: oral agents (cephalexin, dicloxacillin) 3. Keloid Pathologic scar formation with excess collagen synthesis Predilection to darker skin Intralesional corticosteroid injection Cryotherapy 4. Folliculitis Dome shaped pustule, infection at the hair follicle Pathogens: normal flora Antiseptic, topical antibacterial (fucidin) Oral Cloxacillin 7-10 days Samuel Freire da Silva, MD, Atlasdermatologico 3

4 5. Erysipelas Infection in deeper layers of skin, invades dermal lymphatics and causes bacteremia, fever/ chills. Bright, red, hot, well demarcated borders, swollen Pathogens: Strep > Staph, blood cultures for definitive Dx 1 st line: cefazolin, cloxacillin, penicillin 2 nd line: cephalexin, clindamycin 6. Shingles/ Herpes zoster (VZV) Unilateral eruption occurring 3-5 days after pain/paresthesia of dermatome Pathogens: VZV reactivation acyclovir/ famciclovir seems to reduce the incidence of postherpetic neuralgia if initiated within 72 hrs 7. Molluscum contagiosum Central umbilicated dome- shaped lesion Common in children (and in immunocompromised) Pathogens: Poxvirus (fun fact: largest DNA virus) Reassure Cryotherapy with liquid nitrogen Topical keratolytic (cantharidin) Curettage 4

5 8. Erythema infectiosum (Fifth disease) Initially flu- like symptoms with fever Raised, uniform maculopapular rash Distribution: cheeks, chin, forehead with circumoral sparing, can affect trunk and extremities Pathogens: parvovirus B19 (fun fact: smallest DNA virus) supportive 9. Hand- foot- mouth disease (HFMD) Painful, red, non- pruritic blister- like lesions Associated with fevers, malaise, sore throat Pathogens: coxsackievirus type A supportive (hygiene, pain relief) Three history facts Any pattern 5

6 10. Pityriasis rosea Typically starts with a single patch and then disseminates in a Christmas tree pattern Pathogen: Unknown viral fungal (drug like reactions can mimic this) Self resolving in 6-8 weeks if symptomatic, treated with steroids or UV light Benign Meningococcal septicemia Petechial non- blanching rash (from toxin that leads to blood extravasation) Pathogen: N. meningitidis, S. Pneumoniae Diagnosis: start treatment! Do not wait for tests! CBC, blood C&S, Lumbar puncture for CSF cell count/ differential medical emergency! Empiric IV antibiotics (do not delay until CT/ LP)-> Dexamethasone IV started early. Prevention: immunization of children for H. influenzae, S. pneumoniae, N. meningitidis (in some cases in adults as well) Prophylaxis: rifampin or ciprofloxacin for close contacts Necrotizing fasciitis Rapidly spreading deeper tissue infection Ø limb and life threatening!!! Pain out of proportion to clinical findings and beyond the border of erythema Pathogen: usually anaerobic bacteria or Strep Pyogenes, CT if suspected myonecrosis (when CK is high) Rigorous resuscitation + urgent consult with ID. Multiple surgical debridements-> remove all necrotic tissue IV antibiotics 6

7 13. SJS/ TEN Urgent vs non- urgent Steven- Johnson Syndrome (SJS) Toxic Epidermal Necrolysis (TEN) Lesion Etiology Course & prognosis Manageme nt Erythema multiforme with ++ mucosal involvement. Sheet- like epidermal detachment (Nikolsky sign) of <10 BSA 15% drug related (allopurinol, penicillins, anticonvulsants, sulfonamides). Occurs 1-3 weeks post drug exposure fever 4-6 week course, 5% mortality Regrowth of epidermis in 3 weeks. Prolonged hospitalisation, withdraw offending drug, IV fluids, infection prophylaxis, corticosteroids (controversial), consider IVIG Severe MM involvement, blistering, more severe form of SJS with > 30% BSA, Nikolsky sign + 50% are definitely drug related, <10% due to viral infection, immunization fever, unwell 30% mortality due to fluid loss, secondary infection As for SJS, admit to burn unit, debride frankly necrotic tissue, consider IVIG Life-threatening rashes: dermatologic signs of four infectious diseases. Mayo Clin Proc. 1999;74: Toxic shock syndrome Acute onset, fever, hypotension, involvement of 3 or > systems: GI: vomiting, diarrhea, hepatic failure MSK: myalgias, increased CK CNS: disorientation Pathogenesis: reaction to a toxin on the surface of Staph (strep) Risk factors: Staph: nasal packing, tampon use, wound infection Strep: minor trauma, preceding viral infection (chickenpox) supportive- fluid resuscitation, antibiotics Pemphigus vulgaris Autoantibodies to desmoglein : Bullae that rupture Mouth involvement Most characteristic Nikolsky sign (loss of skin from mild pressure) Pathogenesis: idiopathic, drug-induced, autoimmune without Rx pemphigus is a fatal disease Systemic steroids (prednisone) Azathioprine to wean the pt off steroids Rituximab (anti- CD20 Ab) or IVIG in refractory cases 7

8 16. Anaphylactic rash Rash with: Hemodynamic instability: hypotension, tachycardia Respiratory distress: SOB, wheezing, swollen lips, face, tongue Pathogenesis: immediate IgE mediated hypersensitivity emergent airway protection if needed Epinephrine Antihistamines: diphenhydramine (H1 blockers) and Ranitidine (H2 blocker) Glucocorticoids: hydrocortisone, methylprednisolone Another contagion with the strawberry tongue saki-disease.html Kawasaki disease Fever > 5 days + CREAM (Conjunctivitis, Rash, Edema/ erythema (hands and feet), Adenopathy, Mucosal involvement ) Pathogenesis: acute vasculitis of medium size vessels, unknown etiology High dose of ASA while febrile and then low dose ASA IVIG-> reduces risk of coronary aneurysm formation Baseline echo and follow up at 6 weeks Rocky Mountain spotted fever (RMSF) Influenza- like prodrome: acute onset fever, headache, myalgias, anorexia, nausea, vomiting Macular rash appears on day 2-4 of fever Pathogen: Rickettsia Rikettsii, vector- tick (summer months) Diagnosis: serology- indirect fluorescent Ab test Doxycycline, usually 7 day course 8

9 19. Endocarditis Infection of endocardium - leads to fever and murmurs Pathogen: o acute: Staph. Aureus o subacute: Viridans strep, culture negative- coxiella burnetti or bartonella Risk factors: valve abnormalities, IV drug use Diagnosis: best initial test is blood culture (99% sensitive) If negative blood culture, but risks-> echo to look for vegetation Best empiric choice is vancomycin and gentamicin Henoch- Schonlein purpura (HSP) Systemic vasculitis associated with classic triad: GI: Abdominal pain, melena Skin: palpable purpura on buttock/ legs MSK: Arthralgia Pathogenesis: vasculitis secondary to IgA complex deposition, associated with IgA nephropathy Most cases resolve spontaneously Condition abnorm al vital signs Erysipelas Meningococce mia To summarize... Toxic appearan ce Sever e pain Diffuse erythema/ sloughing mucosal/ oral lesion Petechiae/ purpura Anaphylaxis Endocarditis Nec fasciitis TSS Other organ system involvement TEN Ø Bacteremia + chills + fever + involvement of dermis and lymphatics Clinically sick pt + petechial rash + stiff neck 9

10 Ø Respiratory + cardiovascular compromise +/ - Hx of allergy Fever + new murmur + risk factors +/- the following findings: Janeway lesions Roth s spots Osler nodes Splinter hemorrhage Ø Rapidly spreading deep tissue infection + pain out of proportion to clinical findings + tenderness beyond border of erythema Ø Diffuse sheet- like epidermal detachment + >30% BSA involved + MM affected Mucosal involvement, large blistering Ø Desquamation of palms & soles + fever + sbp < or > organ system involvement 10

11 Thank you! References Chen et al. (2011) Toronto Notes: Comprehensive medical reference & review for MCCQE I and USMLE II. Dermatology, Tao Le et al. (2014) First Aid for the USMLE Step I Lowell et al. (2012) Fitzpatrick's Dermatology in General Medicine, 8e Bolognia Et al (2015) Dermatology 4e Alikhan et al. (2016) Review of Dermatology 11