Disclosures Name That Rash or Lesion: Dermatology Across Lifespan ►►Grants: Novartis, DaiichiDaiichi--SankyoSankyo ►►Speaker Bureau: OrthoOrtho--McNeil,McNeil, Wendy L. Wright, MS, RN, ARNP, FNP, FAANP Abbott, Novartis, GSK, Sanofi--Pasteur,Sanofi Pasteur, DSI, Takeda, Merck Adult/Family Nurse Practitioner Owner ––WrightWright & Associates Family Healthcare Owner ––AndersonAnderson Family Healthcare Partner ––PartnersPartners in Healthcare Education
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Fifth’s Disease Objectives (Erythema Infectiosum) Upon completion of this lecture, the Human Parvovirus B19 participant will: ––OccursOccurs in epidemics 1. Identify various pediatric dermatology ––OccursOccurs year round: Peak incidence is late winter and conditions early spring 2. Discuss those dermatology conditions Most common in individuals between 55--15years15years of age that require an immediate referral ––PeriodPeriod of communicability believed to be from exposureexposure 3. Develop an appropriate plan for to outbreak of rash evaluation, treatment, and followfollow--upup of the ––IncubationIncubation period: 5--105 10 days ––CanCan cause harm to pregnant women and individuals who various lesions Wright, 2012 Wright, 2012 are immunocompromised
Fifth’s Disease Fifth’s Disease (Erythema Infectiosum) (Erythema Infectiosum)
Low grade temp, malaise, sore throat Physical Examination Findings ––MayMay occur but are less common ––LowLow grade temperature 3 distinct phases ––FacialFacial redness for up to 4 days ––ErythematousErythematous cheeks ––FishnetFishnet like rash within 2 days after facial redness Nontender and wellwell--defineddefined borders ––Fever,Fever, itching, and petecchiae ––NetlikeNetlike rash Petecchiae stop abruptly at the wrists and ankles Erythematous lesions with peripheral white rims ––HandsHands and feet only RashRash--remitsremits and recurs over 2 week period
Wright, 2012 ––PetecchiaePetecchiae on handsWright, and2012 feet
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Fifth’s Disease Fifth’s Disease (Erythema (Erythema Infectiosum) Infectiosum)
Diagnosis/Plan Diagnosis/Plan ––WasWas contagious before rash appeared therefore, no ––ParvovirusParvovirus IgM and IgG isolation needed ––IgM=MiserableIgM=Miserable and is present in the blood Spread via respiratory droplets from the onset up to 6 months ––SymptomaticSymptomatic treatment ––PatientPatient education--I.e.education I.e. contagion, handwashing ––IgG=GoneIgG=Gone and is present beginning at day ––CanCan cause aplastic crisis in individuals with hemolytic 8 of infection and lasts for a lifetime anemias ––CBCCBC--MayMay show a decreased wbc count ––ConcernConcern regarding: miscarriage, fetal hydrops ––Adults:Adults: arthralgias
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Hand, Foot, and Mouth Disease cdc.gov
(Coxsackie Virus) From November 7, 2011, to February 29, 2012, CDC received reports of 63 persons with signs and symptoms of HFMD or with fever and atypical rash in Caused by the coxsackie virus A16 Alabama (38 cases), California (seven), Connecticut (one), and Nevada (17). Most common in children Coxsackievirus A6 (CVA6) was detected in 25 (74%) of those 34 patientspatients Rash and fever were more severe, and hospitalization was more common 22--66 day incubation period than with typical HFMD. Occurs most often in late summersummer--earlyearly fall Signs of HFMD included fever (48 patients [76%]); rash on the hands or feet, or in the mouth (42 [67%]); and rash on the arms or legs (29 [46%]), face (26 Symptoms [41%]), buttocks (22 [35%]), and trunk (12 [19%]) Of 46 patients with rash variables reported, the rash typically was ––LowLow grade fever, sore throat, and generalized maculopapularmaculopapular;; vesicles were reported in 32 (70%) patientspatients malaise Of the 63 patients, 51 (81%) sought care from a clinician, and 12 (19%) were hospitalized. Reasons for hospitalization varied and included dehydration ––LastLast for 1--21 2 days and precede the skin lesions and/or severe pain ––20%20% of children will experienceWright, 2012 lymphadenopathy No deaths were reported Wright, 2012
Wright, 2012 2 Hand, Foot, and Mouth Disease Hand, Foot, and Mouth Disease (Coxsackie Virus) (Coxsackie Virus)
Physical Examination Findings Physical Examination Findings ––OralOral lesions are usually the first to appear ––Hand/feetHand/feet lesions 90% will have As they evolve ––maymay evolve to form small thick ––LookLook like canker sores; yellow ulcers with red halos gray vesicles on a red base ––SmallSmall and not too painful May feel like slivers or be itchy ––WithinWithin 24 hours, lesions appear on the hands and feet 33--77 mm, red, flat, macular lesions that rapidly becomebecome pale, white and oval with a surrounding red halo
Resolve within 7 days Wright, 2012 Wright, 2012
Hand Foot and Mouth Hand Foot and Mouth Disease Disease
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Hand, Foot, and Mouth Disease Hand, Foot, and Mouth Disease (Coxsackie Virus) (Coxsackie Virus) Plan Plan ––Diagnostic:Diagnostic: None ––EducationalEducational ––TherapeuticTherapeutic Very contagious (2d before --22 days after eruption begins) Tylenol Entire illness usually lasts from 2 days ––11 week Warm baths Reassurance Oragel or Benadryl/Maalox No scarring
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Wright, 2012 3 Pityriasis Rosea Pityriasis Rosea
Etiology Symptoms ––Common,Common, benign skin eruption ––RashRash initially begins as a herald patch ––OftenOften mistaken for ringworm ––EtiologyEtiology unknown but believed to be viral ––29%29% have a recent history of a viral infection ––SmallSmall epidemics occur at frat houses and military ––Asymptomatic,Asymptomatic, salmon colored, slightly itchy rash bases Signs ––FemalesFemales more frequently affected ––ProdromeProdrome of malaise, sore throat, and fever may precedeprecede ––75%75% occur in individuals between 10 and 35; ––HeraldHerald patch: 2--10cm2 10cm oval--roundoval round lesion appears first higheset incidence: adolescents ––MostMost common location is the trunk or proximal extremitiextremitieses ––2%2% have a recurrence
––MostMost common during winterWright, 2012 months Wright, 2012
Pityriasis Rosea Pityriasis Rosea
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Pityriasis Rosea Pityriasis Rosea
Signs ––EruptiveEruptive phase Signs (continued) Small lesions appear over a period of 11--22 ––77--1414 days after the herald patch weeks ––LesionsLesions are on the trunk and proximal ––Fine,Fine, wrinkled scale extremities ––SymmetricSymmetric ––CanCan also be on the face ––AlongAlong skin lines ––LooksLooks like a drooping pine tree ––FewFew lesions--hundredslesions hundreds ––LesionsLesions are longest in horizontal dimension Wright, 2012 Wright, 2012
Wright, 2012 4 Pityriasis Rosea Pityriasis Rosea
Plan Diagnosis ––TherapeuticTherapeutic ––HistoryHistory and physical examination Antihistamine Topical steroids Plan Short course of steroids although, may not respond ––DiagnosticDiagnostic Sun exposure Can do a punch biopsy if etiology uncertain Moisturize ––EducationalEducational ––PathologyPathology is often nondiagnostic Benign condition that will resolve on own ––Report:Report: spongiosis and perivascular round ––MayMay take 3 months to completely resolve cell infiltrate No known effects on the pregnant woman Consider an RPR to rulerule--outout syphilis Reassurance Wright, 2012 Wright, 2012
Impetigo Impetigo
Contagious, superficial skin infection Symptoms: Caused by staphylococci or streptococci ––RashRash that will not go away ––StaphStaph is the most common cause ––BeginsBegins as a small area and then increases in size ––MakesMakes entrance through small cut or abrasion ––Yellow,Yellow, crusted draining lesions ––ResidesResides frequently in the nasopharynx Physical Examination Findings Spread by contact ––SmallSmall vesicle that erupts and becomes yellow--yellow More common in children, particularly on the brown nose, mouth, limbs ––Initially,Initially, looks like an inner tube ––SelfSelf--limitinglimiting but if untreated may last weeks to ––CrustCrust appears and if removed, is bright red and Wright, 2012 Wright, 2012 months inflamed
Impetigo Impetigo
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Wright, 2012 5 Impetigo Impetigo
Physical Examination Findings ––22--88 cm in size Diagnosis ––Diagnostic:Diagnostic: Culture ––MustMust absolutely consider MRSA ––Therapeutic:Therapeutic: Bactroban vs. Altabax 11stst generation cephalopsporin vs. TMP/SMX Let’s discuss MRSA
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Impetigo
Educational CA --MRSAMRSA ––GoodGood handwashing and hygiene ––NoNo school/daycare for 24--4824 48 hours ––WashWash sheets and pillowcases ––MonitorMonitor for serious sequelae
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CACA--MRSAMRSA CACA--MRSAMRSA First identified in the 1940’s; first US case -- 1968 ––CACA--MRSAMRSA is distinctly different than the MRSA First domestic cluster of cases identified in hospitals identified in 1982 in Detroit, Michigan ––MostMost CA--MRSACA MRSA are known as USA300 or USA400 ––IVIV drug users whereas hospital infections are USA100, USA500 1992, 2 ndnd cluster among IV drug users Since 1990, the burden on society has increased substantially Most infections are located in the soft tissue and present as carbuncles, furuncles or abscessesWright, 2012 Wright, 2012
Wright, 2012 6 CACA--MRSAMRSA CACA--MRSAMRSA
Males are affected more often than females Affects the very young and old disproportionately Blacks are also affected at greater rates than whites Recurrent antimicrobial usage may be a risk factor Exposure to farm animals and even household
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CACA--MRSAMRSA CACA--MRSAMRSA
Current estimates: Most CACA--MRSAMRSA infections are not ––2525 ––30%30% of people carry colonies of usually severe or associated with staphylococci in their noses deaths although the CA strains are ––<< 2% are colonized with MRSA believed to be more virulent than the hospital strains However, current yearly estimates are: ––95K95K invasive infections ––19K19K deaths
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CA --MRSAMRSA CACA--MRSAMRSA
mecA gene 2002 ––handfulhandful of cases of the ––ThisThis is where the resistance originates bacterium which is resistant to with MRSA vancomycin ––PCNPCN can’t bind at its target A lot of cross resistance to beta lactam antibiotics: PCN and cephalosporins particularly in the USA300 strain which is the CACA--MRSAMRSA strain
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Wright, 2012 7 Treatment for Statistics/Treatment in My Uncomplicated CACA--MRSAMRSA Community No significant risk factors for adverse outcomes I&D is the treatment of choice; antibiotics may 37% of staph infection at DHMC –– not be necessary MRSA For those in whom antibiotics should be Nationally, approximately 31% are considered: MRSA ––SignificantSignificant pain CACA--MRSAMRSA antibiotic susceptibility ––CellulitisCellulitis ––50%50% will be resistant to clindamycin ––RapidRapid progression Bactrim has best coverage/sensitivity: ––ImmunosuppressionImmunosuppression 9696--98%98% Wright, 2012 Wright, 2012 ––ComorbiditiesComorbidities ––ImportantImportant for clinicians to obtain own antibiogram for communities in which you
Treatment of CACA--MRSAMRSA Treatment of CACA--MRSAMRSA Skin infections: Obtain culture ––TMP/SMXTMP/SMX Should consider local antibiograms in selection ––ClindamycinClindamycin (Monitor closely for resistance; D--ZoneD Zone of antimicrobials test) Skin infections: ––TetracyclinesTetracyclines (avoid under 8 years of age) ––ConsiderConsider beta--lactambeta lactam (PCN or Cephalo) in an ––RifampinRifampin ––addadd on to other agents individual with mild infection and low rates of CACA-- ––LinezolidLinezolid MRSA in your community (generally thought of as < 10 ––15%)15%) ––AvoidAvoid fluoroquinolones (increasing resistance) Guilbeau, J.R. and Fordham, P.N. Evidence-Based management and Treatment of Outpatient Community- Guilbeau, J.R. and Fordham, P.N. Evidence-Based management and Treatment of Outpatient Community- Associated MRSA. The Journal for Nurse Practitioners. 2010; Vol 6(2):140-145 Associated MRSA. The Journal for Nurse Practitioners. 2010; Vol 6(2):140-145 Wright, 2012 Wright, 2012
Treatment and Eradication Strategies: Recurrent Carriage of CACA--MRSAMRSA infections GOOD handwashing Treatment recommended for individuals with recurrent infection Treatment with Bactrim,clinda,Bactrim,clinda , TCN, Linezolid ––ConsiderConsider addition of rifampin ––ConsiderConsider ID consult before treatment ––MupirocinMupirocin 2% each nostril two times daily x 5 days Bathe with disinfectants along with daily cholorhexidine 4% bath. ––HibiclensHibiclens,, phisodex,phisodex , cloroxbleach ––AlternativeAlternative Utilize topical disinfectants Doxycycline 100 mg bid or TMP/SMX DS + rifampin 300 ––PurellPurell mg every 12 hours x 5 days ––MupirocinMupirocin ––seeingseeing resistance Guilbeau, J.R. and Fordham, P.N. Evidence-Based management and Treatment of Outpatient Community- Associated MRSA. The Journal for Nurse Practitioners. 2010; Vol 6(2):140-145 Wright, 2012 Wright, 2012
Wright, 2012 8 Another Option More Natural Options
Mupirocin nasal ointment plus bleach Stay tuned… baths (one tablespoon of bleach in 1 ––LemongrassLemongrass essential oil has been shown quart of water) to inhibit all MRSA colony growth ––AbleAble to decolonize the skin ––TeaTea tree oil has also been shown effective Some strains of MRSA (USA300 MRSA clones) are resistant to ––FrenchFrench clay is also being studied mupirocin
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Additional Who Should Be Considerations Hospitalized? Two or more of the following: CA --MRSAMRSA ––FeverFever > 100.4 ––CanCan colonize in animals; household pets ––WbcWbc count: > 13,000/uL ––ConsiderConsider animal treatment with recurrent ––BandsBands > 10% disease ––HandHand cellulitis Fomites ––FacialFacial cellulitis ––MayMay be a source of CA --MRSAMRSA ––ImmunocompromiseImmunocompromise ––CanCan live > 5 weeks on vinyl or block toys ––FailingFailing outpatient therapy ––CanCan live on towels for 7 ––1010 days ––AgeAge > 70 years of age
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Contact Dermatitis: Clinical Pearls Rhus Dermatitis Poison ivy is not spread by scratching Rhus Dermatitis ––PoisonPoison ivy, poison oak and poison sumac produce No oleoresin is found in the vesicles and more cases of contact dermatitis than all other therefore, can not be spread by contactants combined scratching ––OccursOccurs when contact is made between the leaf or Lesions will appear where initial contact internal parts of the roots and stem and the individual with plant occurred Can occur when individual touches plant or an Resin needed to be washed from skin animal does and then touches human within 15 minutes of exposure to ––EruptionEruption can occur within 8 hours of the contact but decrease risk of condition may take up to 1 week toWright, occur 2012 Wright, 2012
Wright, 2012 9 Clinical Presentation Contact Dermatitis
Clinical presentation ––CharacteristicCharacteristic linear appearing vesicles are likely to appear first ––OftenOften surrounded by erythema ––IntenselyIntensely itchy ––LesionsLesions often erupt for a period of 1 week and will last for up to 2 weeks ––MoreMore extensive and widespread presentation can occur with animal exposures or burning of
the plants / smoke exposureWright, 2012 Wright, 2012
Contact Dermatitis Treatment
Cool compresses 15 ––3030 minutes three times daily Topical calamine or caladryl lotions Zanfel (OTC) wash ––bindsbinds urushiol oil and removes from body/blisters ––75%75% decrease in itching and rash within 24 hours per package Colloidal oatmeal baths (AVEENO) Wright, 2012 once daily Wright, 2012
Treatment FollowFollow--upup Oral antihistamines Monitor for secondary infections ––MayMay wish to use sedating antihistamines at Impetigo bedtime ––StaphStaph vs. strep Topical corticosteroids ––MRSAMRSA ––AvoidAvoid usage on the face Education: Oral prednisone vs. injectable Kenalog or ––LesionsLesions will decrease over a 2 week period similar ––MayMay continue to erupt over 48 hours despite ––2020 mg two times daily x 7 days steroid administration ––KenalogKenalog 40 mg injection (IM) ––NotNot spreading lesions with rubbing or scratching
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Wright, 2012 10 Hot Tub Folliculitis Clinical Presentation
Inflammation of the hair follicle Caused by infection which occurs within 8 hours –– One or more pustules may first appear 5 days of using contaminated hot tub or whirlpool Fever may or may not be present; Unfortunately, showering after exposure provides usually low grade if it does occur no protection Pseudomonas is the most common cause of hot Malaise and fatigue may accompany tub folliculitis the outbreak May also be caused by Staphylococcus, but Pustules may have wide rims of unusual erythema ––MSSAMSSA or MRSA Wright, 2012 Wright, 2012
Hot Tub Folliculitis Treatment
Culture of lesions is likely warranted White vinegar wet compresses ––2020 minutes on three x daily may provide significant benefit Oral Antibiotics ––CiprofloxacinCiprofloxacin is preferred agent if hot tub folliculitfolliculitisis is suspected due to pseudomonas coverage Discuss contagiousness ––NoNo evidence that it is spread person --personperson
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Case Study Case Study S:TM is a 6464--yearyear--oldold Caucasian male who presents with Allergies: NKDA a painful rash located on his right buttock. ––DescribesDescribes the rash as red and blistered PMH: dyslipidemia; hypertension; obesity, ––HasHas been present x 96 hours and is in for an evaluationevaluation because the pain is severe. allergic rhinitis ––PainPain is “9” on 0 ––1010 scale. Has tried oral OTC medicatmedicationsions Social history: 30 pack year history of without significant improvement. Pain is described as a burning sensation; deep in his buttock. cigarette smoking; none x 10 years; ––DeniesDenies precipitating factors. Pain began approx 2 daysdays bbeforeefore the rash appeared. Denies fever, chills, new soaps, lotions, changes Machinist; happily married x 40+ years in medications. Medications: atorvastatin 40 mg 1 po qhs; amlodipine 5 mg 1 po qhs; loratidine 10mg 1 po qd; aspirin 81 mg 1 po qam; various vitamins
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Wright, 2012 11 Case Study Case Study O: T:97.8; P: 94; R:18; BP: 148/90 O: PE continued ––Skin:Skin: p/w/d; approximately 15--2015 20 vesicles ––Back:Back: From: no tenderness, erythema, masses located on right buttock overlying an ––Abdomen:Abdomen: Soft, large; + BS; no masses, erythematous base; vesicles are clustered tenderness, hsm but without obvious pattern; no streaking, ––Neuro:Neuro: intact including light touch, pain, vibratoryvibratory petecchiae. Few scattered vesicles on to right lower extremity; heel, toe walking intact posterior aspect of right thigh; no lesions on left buttock or leg + Allodynia ––Clothing,Clothing, light touch, cool object ––Hips:Hips: FROM: no tenderness, erythema, masses + Hyperalgesia ––PainfulPainful stimuli elicited significant pain
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Examples of Herpes Zoster Herpes Zoster
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Acute Herpes Zoster Herpes Zoster Highly contagious DNA virus which during the varicella infection (primary infection) gains access into the dorsal root ganglia Virus remains dormant for decades and is reactivated when an insult occurs to the individual’s immune system ––Examples:Examples: HIV, chemotherapy, illness, stress, corticosteroid usage
Wright, 2012 Wright, 2012 Dr P. Marazzi , ScienceScience Photo Library.Library. Image usedused withwith permissionpermission.
Wright, 2012 12 Incidence and Prevalence Risk Factors Increasing age (50(50--6060 years and beyond) 3 million cases of chickenpox yearly ––DiseaseDisease of childhood Varicella infection when < 2 years of age 600,000 --11 million cases of herpes zoster Immunosuppression each year in the United States Stress (controversial) ––TendsTends to be more of a disease of aging Trauma ––ByBy age 80, 20% of us will have zoster at some point in our lifetime Malignancies ––MenMen = Women ––25%25% of patients with Hodgkin’s will develop zoster 11
www.niaid.nih.gov/shingles/cq.htm 1Stankus, S. et. Al. Management of Herpes Zoster and Postherpetic Neuralgia. Am Fam Wright, 2012 Wright, 2012 Physician 2000;61:2437-44, 2447-8)
Goals of Treatment Acute Treatment Options Antiviral Treat acute viral infection ––Goal:Goal: Reduce viral reproduction Corticosteroids ––ShortenShorten course ––InitiallyInitially postulated that these reduce viral replication; recent studies have not found this ––ReduceReduce lesions to be true Treat acute pain ––However,However, they do decrease pain Pain Management Prevent complications ––TopicalTopical agents ––AntiAnti--inflammatoryinflammatory agents ––PostherpeticPostherpetic neuralgia ––NarcoticsNarcotics
Wright, 2012 Postherpetic neuralgiaWright, 2012prevention www.aad.org/pamphlets/herpesZoster.html
Antiviral Treatment Controlled Trials of Antiviral Options Agents in Herpes Zoster Ideally, want to begin within the first 72 % of patients 3 months 6 months hours of the eruption as benefits may be with PHN at: reduced if started after that Acyclovir vs. 25% vs. 54% 15% vs. 35% Placebo These medications decrease duration of the rash and severity of the pain Valacyclovir vs. 31% vs. 38% 19.9% vs. 25.7% Acyclovir ––StudiesStudies vary as to how much these products actually reduce the incidence of postpost-- Famciclovir vs. 34.9% vs. 49.2% 19.5% vs. 40.3% herpetic neuralgia Placebo
1Stankus, S. et. Al. Management of Herpes Zoster and Postherpetic Neuralgia. Am Fam Physician 2000;61:2437-44, 2447-8) Wright, 2012 Adapted from Johnson RW. J AntimicrobWright, 2012 Chemother. 2001;47:1-8.
Wright, 2012 13 Corticosteroids Pain Often utilized despite mixed results in clinical trials Pain associated with herpes zoster can range from mild ––severesevere Prednisone, when used with acyclovir, in one study reduced pain associated with Clinician must tailor pain medication options herpes zoster based upon individual presentation Corticosteroids are currently recommended for individuals over 50 years of age with HZ Dosage: ––3030 mg bid x 7 days; 15 mg bid x 7 days; 7.5 mg
1 11 bidStankus, x 7 S. days et. Al. Management of HerpesWright, Zoster 2012 and Postherpetic Neuralgia. Am Fam Wright, 2012 Physician 2000;61:2437-44, 2447-8)
Pain Management Acute Pain Management Topical Agents Oral Agents ––CalamineCalamine lotion to lesions 2 ––3x/day3x/day ––AcetaminophenAcetaminophen ––BetadineBetadine to lesions qd Has not been shown to be effective in trials) ––CapsaicinCapsaicin cream once lesions crusted 3 –– ––IbuprofenIbuprofen or similar 5x/day Not likely to be effective with neuropathic pain ––TopicalTopical lidocaine 5% patch for 12 hours at a time Nerve Blocks once lesions are crusted ––HaveHave been shown to be effective for many individuals with severe pain in some trials; other trials --ineffectiveineffective
1 Stankus, S. et. Al. Management of HerpesWright, Zoster 2012 and Postherpetic Neuralgia. Am Fam Wright, 2012 Physician 2000;61:2437-44, 2447-8)
FollowFollow--upup
And…the use of medications Monitor for secondary infections such as TCA’s, gabapentingabapentin,, Monitor for evidence of pregabalinpregabalin,, oxycodone and postherpetic neuralgia tramadol during the acute phase Monitor for adverse impact on of HZ decrease pain but also may quality of life also reduce the risk of PHN
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Wright, 2012 14 Capsaicin Patch Application Instructions
Capsaicin 8% ((QutenzaQutenza)) patch Indications: PostPost--herpeticherpetic neuralgia Draw circle around area to be covered ––ApplyApply to most painful skin areas Cleanse area first and thoroughly dry ––MayMay apply up to 4 patches at same time PrePre--treattreat area with local anesthetic first ––ShouldShould wear gloves when applying Once anesthetized, remove anesthetic ––ShouldShould only be applied by a healthcare and cleanse professional ––RemainsRemains on x 60 minutes only
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Erythema Chronicum Migrans Capsaicin Efficacy: ––ProvidesProvides up to 12 weeks of reduced pain with a Etiology 1 hour patch application ––CausedCaused by a spirochete called Borrelia Borgdorferi Warnings ––TransmittedTransmitted by the bite of certain ticks (deer, ––MayMay elevate BP; should monitor during whitewhite--footedfooted mouse) treatment ––1st1st cases were in 1975 in Lyme, Connecticut ––DoDo not apply to open skin ––OccursOccurs in stages and affects many systems Side effects ––ChildrenChildren more often affected than adults ––ApplicationApplication site pain (42% vs. 21%)
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Erythema Chronicum Migrans This is NOT a Lyme Bearing Tick
Etiology ––SummerSummer--highesthighest incidence ––80008000 cases/year in the US ––2020 countries, 6 continents ––CanCan be passed to fetus in utero
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Wright, 2012 15 Erythema Chronicum Migrans Lyme Bearing Tick Symptoms ––33--2121 days after bite ––StageStage 1 Rash (present in 7272--80%80% of cases)--slightlycases) slightly itchy Lasts 33--44 weeks Mild flu like symptoms (50% of time) Migratory joint pain ––StageStage 2 Neurological and cardiac symptoms ––StageStage 3 Arthritis, chronic neurological symptoms
Wright, 2012 Make take years to get toWright, this 2012 stage
Erythema Chronicum Migrans Erythema Migrans Signs ––Rash:Rash: Stage 1 Begins as a papule at the site of the bite Flat, blanches with pressure Expands to form a ring of central clearing No scaling Slightly tender ––Arthralgias:Arthralgias: Stage 2 Asymmetric joint erythema, warmth, edema Knee is most common location Wright, 2012 Wright, 2012
Erythema Migrans Erythema Chronicum Migrans
Signs ––SystemicSystemic symptoms: Stage 3 Facial palsy Meningitis Carditis Diagnosis ––R/OR/O Ringworm (Tinea Corporis)
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Wright, 2012 16 Erythema Chronicum Migrans Erythema Chronicum Migrans
Plan Plan ––Diagnostic:Diagnostic: ––TherapeuticTherapeutic Sed rate: normal until stage 2 Amoxicillin 500mg tid x 21 days Lyme Titer Doxycycline 100 mg 1 po bid x 21 days ––IGM:IGM: Appears first: 3--63 6 weeks after infection begins If in endemic area and tick is partially engorged, ––IGG:IGG: Positive in blood for 16 months may treat with doxycycline 200 mg x 1 dose with ––HighHigh rate of false negatives early in the disease food ––LymeLyme Western Blot
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Erythema Chronicum Migrans Necrotizing Fasciitis
Educational Severe, deep, necrotizing infection ––HalfHalf of the patients continue to experience h/a, Involves subcutaneous tissue down into the arthralgias and fatigue after treatment muscles ––TickTick repellant Spreads rapidly ––LightLight clothing Caused by Group A Beta Hemolytic Strep, ––CheckCheck children and pets and remove promptly Staph, Pseudomonas, E Coli ––ClosedClosed toe shoes Mortality: 88--70%70% depending upon organism ––CombComb hair and rapidity of treatment Disfigurement common Wright, 2012 Wright, 2012
Necrotizing Fasciitis Necrotizing Fasciitis Symptoms Physical Examination Findings ––UsuallyUsually occurs after surgery, traumatic wounds, injection sites, cutaneous sores ––TenderTender ––GeneralizedGeneralized body aches, fever, irritability ––BullaeBullae with purulent center which ruptures quickly ––Key:Key: Red area of skin that is severely painful (It ––BlackBlack eschar appears and the pain decreases is out of proportion to findings) ––SystemicSystemic symptoms begin ––LegLeg is most common location Physical Examination Findings ––1st1st appears as local area of redness that looks
like cellulitis Wright, 2012 Wright, 2012
Wright, 2012 17 Necrotizing Fasciitis Necrotizing Fasciitis
Plan ––Diagnosis:Diagnosis: Culture of wounds, blood cultures, biopsy of area, CBC with differential, urinalysis ––Therapeutic:Therapeutic: HOSPITAL ADMISSION ––Educational:Educational: Good wound hygiene
Bullae: Below these lesionsWright, 2012is necrotic tissue Wright, 2012
StevensStevens--JohnsonJohnson Syndrome StevensStevens--JohnsonJohnson Syndrome
Distinct, acute hypersensitivity syndrome Mortality: 55--25%25% Many causes: Drugs, bacteria, viruses, foods, immunizations LongLong--termterm complications are common Also known as Bullous Erythema Multiforme Face almost always involved and mouth StevensStevens--JohnsonJohnson Syndrome is thought to represent always involved the most severe of the erythema multiforme spectrum Entire course: 33--44 weeks Two stages Most common in children aged 2 --1010 ––ProdromeProdrome which lasts 1--141 14 days ––2nd2nd stage: mucosal involvement where at least 2 mucousal surfaces are involved (oral, conjunctival, urethral)
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StevensStevens--JohnsonJohnson Syndrome Erythema Multiforme
Symptoms ––ConstitutionalConstitutional symptoms such as fever, headache, sore throat, nausea, vomiting, chest pain, and cough Physical Examination Findings ––VesiclesVesicles that are extensive and hemorrhagic ––BullaeBullae rupture leaving ulcerations which are covered with membranes ––LeaveLeave large areas of necrosis and skin peels ––LesionsLesions on the conjunctivaWright, 2012 Wright, 2012
Wright, 2012 18 StevensStevens--JohnsonJohnson Erythema Multiforme Syndrome
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StevensStevens--JohnsonJohnson Syndrome StevensStevens--JohnsonJohnson Syndrome
Plan ––MustMust rule--outrule out staphylococcal scalded skin syndrome ––Therapeutic:Therapeutic: HOSPITALIZATION with early opthamological evaluation ––SteroidsSteroids are controversial ––OthersOthers in family may be genetically susceptible ––NeverNever take these medications again
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Diagnosis? Dermatofibroma Linked with______?
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Wright, 2012 19 Squamous Cell Carcinoma Seborrheic Keratosis
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Basal Cell Carcinoma Malignant Melanoma
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Squamous Cell Carcinoma Molluscum Contagiosum
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Wright, 2012 20 Key References BologniaBolognia,, Jean, Joseph L. JorizzoJorizzo,, and Thank You! Ronald P. Rapini.Rapini . Dermatology . 2nd ed. St. Louis, Mo.: Mosby/Elsevier, 2008. Print. HabifHabif,, Thomas P.. Skin disease: diagnosis I Would Be Happy To and treatment . 2nd ed. Philadelphia: Elsevier Mosby, 2005. Print. Entertain Any Questions Hunter, J. A. A., John SavinSavin,, and Mark V. Dahl. Clinical dermatology . 3rd ed. Malden, Mass.: Blackwell Science, 2002. Print.
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Wendy L. Wright, MS, RN, ARNP, FNP, FAANP
603 472472--70977097 (W) 603 472472--2597(F)2597(F) email: [email protected]
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