SKIN AND SOFT TISSUE INFECTIONS

e patient’s immune status, geographic locale, travel history, recent trauma or surgery, previous antimicrobial therapy, lifestyle, hobbies, and animal exposure or bites

VENOUS

LYMPHATIC COMPROMISE FROM PREVIOUS CELLULITIS

PERIPHERAL EDEMA

PREVIOUS RADIATION TO AN AREA

HX OF LYMPH NODE RESECTION

LYMPHEDEMA

OBESITY

TRAUMATIC LACERTION

CHRONIC DERMATOSES -W SKIN BREAKDOWN FROM ECZEMA /MACERATED TINEA PEDIS,BUG BITES SURGICAL WOUND INFECTIONS

THIS IS LEG CELLULITIS

STAPH AUREUS

MRSA

MSSA

HEMOPHILUS INFLUENZAE( CHILDREN MORE COMMON)

>80

PRIOR TRAUMA

UNTREATED FURUNCULOSIS

BURNS

DM

URI ( KIDS)

IMMUNOCOMPROMISE

BUG BITE

LACERATION

USUAL +

PAIN

FEVER

LYMPHADENOPATHY

FISSURING /MACERATION TOE WEBS-CAUSE

HISTORY OF RECURRENT ABSCESSES

ACUTE GOUT

ERYSIPELAS

STASIS DERMATITIS

CONTACT DERMATITIS

FOLLICULITIS

IMPETIGO

VZV

RUPTURED BAKERS CYST

ERYTHEMA MIGRANS

CBC W DIFF-LEUCOCYTOSIS WITH LEFT SHIFT ( BANDS, NEUUTROPHILIA)

CREATININE,

BICARBONATE

CREATININE PHOSPHOKINASE’

CULTURE OF WOUND

GRAM STAIN

BLOOD CULTURE ( SEPSIS )

ESR ( ELEVATED)

IMAGING

CT /MRI IF OM SUSPECTED

MSSA AND B HEMOLYTIC STREPTOCOCCI

CEPHALEXIN 500 MG PO QQID X 5-7 DAYS

MRSA

BACTRIM DS 1 TAB PO 5-10 DAYS , 14 DAYS IF COMPLEX

MRSA PLUS BHS

CLINDAMYCIN 300-450 PO Q 6 X 7 DAYS

MRSA SUSPECTED: HIBICLENS WASHES X 7 DAYS AND MUPIROCIN OINTMENT NARES BID OR TID X 56DAYS

NON PHARM

MOIST HEAT

ELEVATION

F/U

24-48-HOURS AFTER TREATMENT AND AS PT CONDITION DICTATES

MAY BE MRSA IF NOT RESPONDING TO KEFLEX

REFER ID OR ED

INFECTIONS FACE NECK SCALP

SEPSIS

SURGERY IF DRAINAGE NEEDED

IMMUNOCOMPROMISED PTS

folliculitis

superficial infection of hair follicles

lesions small raised erythematous ,occasionally pruritic,<5mm

FURUNCULOSIS

DEEP INFECTION OF FOLLICLE

ROUND TENDER NODULE BECOMES PUSTULE OR PERIFOLLICULAR ABSCESS

NECK FACE BUTTOCKS WAISTLINE BREASTS

CARBUNCULOSIS

DEEP SUPPURATIVE LESION

EXTENDS INTO SC TISSUE

COALESCENCE OF SEVERAL FOLLICLES

PUS

CUTANEOUS ABSCESS: COLLECTION OF PUS WITHIN DERMIS AND DEEPER TISSUES

PAINFUL FLUCTUANT,SURMOUNTED BY PUSTULE

RIM OF ERYTHEMATOUS SWELLING

POLYMICROBIAL W REGIONAL SKIN FLORA-OFTEN STAPH OR MRSA (IDSA)

EPIDERMOID CYST

ERRONEOUSLY CALLED SEBACEOUS CYSTS

NORMAL SKIN FLORA IN A CHEESY KERATINOUS MATERIAL

INFLAMMATION AND PUS OCCURS AS A REACTION TO RUPTURE OF THE CYST WALL AND EXTRUSION OF CONTENTS INTO DERMIS ,RATHER THAN AN INFECTIOUS PROCESS(IDSA)

STAPH AUREUS

MRSA COMMON OUTPATIENT SETTING

PSEUDOMONAS HOT TUB FOLLICULITIS

PITYROSPORUM FOLLICULITIS

F- ALL AGES RECURS-

SHAVING POOR HYGIENE ,WATER EXPOSURE,OCCLUSIVE STEROIDS THX

FU TEENS ADULTS RECURS

POOR HYGIENE, CROWDED , DM

C

MEN>WOMEN , AT RISK IMMUNO OLDER ADULTS, CHRONIC DISEASES

CHORNIC DX, DM ETOH ELDERLY

F SUPERIFICAL HAIR COMES OUT OF FOLLICLE EASY, MILD ERYTHEMA

FC PUSTULE WITH CENTRAL NECROSIS AND CORE OF PUS PAIN INFLAMMATION EDEMA MAY NEED I&D

C

FEVER SLOW DEVELOP SLOUGH DRAINAGE MULTIPLE OPENINGS , NEEDS I&D

PSUEDOFOLLICULITIS

ACNE V

CUTANEOUS CANDIDIASIS

KERTOSIS PILLARIS

FU'

FOLL, CARB, HS PILAR CYSTS

CA

CYSTIC ACNE

EPIDERMAL CYST

FOLL

HS

FISH TANK MYCOBACTERIUM MARINUM

RECURRENT SEVERE

BETADINE OR HIBICLENS DAILY IN FULL SHOWERS 1-3 WEEKS

CHANGE TOWELS AND SHEETS DAILY

HAND WASHING

AVOID HEAT FRICTION

diagnositcs

f #15 scalpel for KOH ASSESS FOR PITYROSPORUM FOLLICULITIS /OR YEAST

Gram stain and culture of pus from carbuncles and abscesses are recommended, but treatment without these studies is reasonable in typical cases (idsa)

do not culture inflamed epidermoid cysts

temperature >38°C or <36°C, tachypnea >24 breaths per minute, tachycardia >90 beats per minute, or white blood cell count >12 000 or <400 cells/µL

ALLOW SPONTANEOUS DRAINAGE,

PREVENT MEASURES LISTED

MOIST WARM COMPRESS

SHAVE GEL HYDRATE VEFORE SHAVING

Lipodermatosclerosis is a chronic inflammatory condition characterised by subcutaneous fibrosis and hardening of the skin on the lower legs.

Lipodermatosclerosis is also known as sclerosing panniculitis and hypodermitis sclerodermaformis.

Depending on the location of infection, the treatment of choice is a combination of surgical management and antibiotics, such as ampicillin or penicillin. Antibiotics that are typically effective against oropharyngeal flora, such as clindamycin and metronidazole, are ineffective against Eikenella species.

NON PURULENT SSTI

OFTEN ON FACE

ON UPPER DERMIS ( PAPILLARY ) AND LYMPHATICS

FACE EARS LOWER EXTREMITIES

SWOLLEN

ORANGE PEEL LOOK

CHILDREN

GERIATRIC

IMMUNE

DM

HIV

EXPOSURE TO ORGANISMS

ALTERATION IN SKIN INTEGRIITY 2/2

TRAUMA

ATOPIC DERMATITIS

ALLERGIC CONTACT DERMATITIS

POSRIASIS

INSECT BITE

EDEMA

ERYTHEMA WITH WELL DEMARCATED BORDERS OF INFLAMMATION

LYMPHATIC STREAKING MAY OCCUR

EDEMA

USU STUFF

PAIN

UNILATERAL

PRURITUS

NEC FAS

DVT

CONTACT DERMATITIS

INSECT BITE

VZV

STASIS DERMATITIS

VBASED ON CLINICAL PRESENTATION

CULTURES RARELY HELPFUL

IMAGING FOR R/O NEC FASC

PYOMYOSITIS AND ABCESS

LABS

CBC ESR CRP

PCN V 500 MG QID X 10 DAYS

PCN ALLERGY MACROLIDE

PAIN MGT

IBUPROFEN

TYLENOL

ID OR SURGERY

RAPID PROGRESSION INFECTION

SIRS

IMMUNOCOMP

AGGRESSIVE SOFT TISSUE LESION

CAUSES NECROSIS MUSCLE FASCIA AND SC TISSUE

INTRODUCED VIA BREAK IN SKIN

OVERLYING TISSUE MAY NOT BE INVOLVEED AND THIS MAY CAUSE DELAY IN TREATMENT

GABHS

STAPH MSSA AND MRSA

HEMOPHILUS INFLUENZA - KIDS

SAME AS ERISYPELAS

• ALCOHOLISM

• 
  

ERYTHEMA

WARMTH

EDEMA

EXCRUCIATING PAIN DISPROPORTIONATE TO WOUND

FEVER >102

TACHYCARDIA

CREPITUS

SKIN BULLAE NECROSIS OR ECCHYMOSIS

THIN FOUL SMELLING DISCHARGE

BLOOD CULTURES IF RAPID PROGRESSION OF MANIFESTATIONS

NON PRAPID

BLOODCULTURES

URGENT SURGICAL EXPLORATION FOR AEROBIC AND ANAEROBIC GRAM STAIN CULTURE AND PATHOLOGY

AGGRESSIVE SX DEBRIDEMENT

IF NOT URGENT

CT

EPIDERMAL /DERMAL JUNCTION FLATTENING

DECREASED BLOOD FLOW

IMMUNOSENESCENCE

2-3 FOLD MORTALITY IN SSTI ELDERLY

BLUE HEALTHY SKIN

LIGHT PURPLE DEHYDRATION

WHITE VITILIGO

RED CORAL CORYNEBACTERIUM MINUTIISSIMUM

YELLOW-GREEN IS PATHOGENIC PSEUDOMONAS

GOUT

OM

GAS GANGRENE

ABSCESS

EPIDIYMITIS

RUPTURED BAKERS CYST

THROMBOPHLEBITIS

ERISYPELAS MORE DEMARCAED AND SUPERFICIAL AND CAN BE ON FACE

PRESENCE OF HEMORRHAGIC BULLAE OR LYMPHANGITIS SUGGEST

STREPTOCOCCAL INFECTION AS OPPOSED TO STAPHYLOCOCCAL INFECTION

YMPHANGITIS SPREADS PROXIMALLY

DEEP SEATED INFECTION EG FASCIITIS, MYOSITIS

SEPTICEMIA

NEPHRITIS

FLUCLOXACILLIN 500 MG 4 X DAY X 7-10 DAYS -BACTERICIDAL ON STREP AND STAPH CHECK IF PCN V

PCN ALLERGY DOXYCYCLINE- SE POWERPOINT

LESIONS ARE SCALING FISSURING/WRINKLING BROWNISH MACERATED

TOES MOST BETWEEN 3RD AND 4TH TOES AND WHITISH COLOR

RESEMBLES TINEA

ERYTHRASMA IS OFTEN 2/2 TINEA PEDIS

WARM HUMID CLIMATE

DM

ELDERLY +IMMUNOCOMPROMISED

FIRST LINE

TOPICAL

BENZOYL PEROCIDES WASH AND 5% GEL

CLINDAMYCIN 2% OR AZOLE CREAMS BID FOR 2 WEEKS

WIDESPREAD ERYTHRASMA

TOPICAL ABX+ TOPICAL

SUSCEPTIBEL TO PCS,IST GEN CEPHALOSPORINS, MYCINS9MACROLIDES

ORAL ERYTHROMYCIN 500MG BID x14 DAYS IS DRUG OF CHOICE

RELAPSES -ORAL TETRACYCLINE 250 MG PO QID X 14 DAYS- NOT PFR PREGNANT WOMEN

COMMON RELAPSES 6-12 MONTHS QUIZLET

RED LEIGHT THERAPY ALTERNATIVE ADJUNCT - LITTLE CLIINICAL DATA TO SUPPORT

EDUCATE ENTIRE FAMILY IN REDUCING RISK OF REPEAT INFECTIONS MINIMISE COLONIZATION

PROPER CLOTHES WASHING

REPLACE SHOES FREQUENTLY

ANTIBACTERIAL WASHES

LOOSE FITTING WICKING CLOTHING

AVOID HUMIDITY

ALUMINUM CHLORIDE DEODOARNAT TO FEET ANECDOTAL

• Wood light examination

• Potassium hydroxide preparation

• Gram-stain

• Culture

DIFF

(1) acanthosis nigricans,

(2) allergic contact dermatitis,

(3) cutaneous candidiasis, and

(4) intertrigo.

TINEA PEDIS

T RUBRUM MOST COMMON

T METAGRAPHYTES

EPIDEROPHYTON FLOCCOSUM

RISK FACTORS

CLOSE CONTACT ANIMALS

WARM CLIMATES

SPORTS

OBESITY

IMMUNOCOMPROMISED/STEROID USE

WELL CIRCUMSCRIBBED

RED SCALY OFTEN ROUND

ARCHIFORM

PRURITIC

KOH SCRAPING

WOODS LAMP

CLOTRIMAZOLE BID

MICONAZOLE OD TO BID

ECONAZOLE

KETOCONAZOLE OD

NAFTIDINE

TERBINAFINE -LAMISIL OD TO BID

JUBLIA

2 WEEKS TREATMENT

ANOTHER SLIDE SAYS 6 WEEKS TREATMENT FOR TINEAPEDIS, 2 WEEKS FOR CANDIDAISIS

TINEA UNGUIUM/ONCHOMYCOSIS

DIABETES

APPEARANCE

KOH PREP

CULTURE

PERIODIC ACIDD-SCHIFF PAS

0-50% NAIL TOPICAL

EFINACONAZOLE -JUBLIA 10% DAILY X 48 WEEKS

CICLOPIROX- PENLAC 8% X 48 WEEKS DONT DC IF CLEARS UP,NEW NAIL MAY SHOW CLEARANCE

>50% INVOLVEMENT , PROXIMAL AND LATERAL

ORAL

TERBANIFINE 250 MG X 6-12 WEEKS

ITRACONAZOLE 200 MG PULSE OR CONTINUOUS RX

NAIL REMOVAL

TERBAINFINE HEPATO AND RENAL TOXICITY- LFT Q 6 WEEKS IF NAUSEA AND ANOREXIA

KETOCONAZOLE PO HEPATOTOXICITY DRUG INTERACTIONS

ITRACONAZOLE CYP 50 SYSTEM CYP3A4- DRUG DRUG INTERACTIONS

MICROSPORUM

TRICHOPHYTON

FFUNGUS GROWS DOWNWARDS IN STRATUM CORNEUM AND INVADES KERATIN

INFECTED HAIR BECOMES BRITTLE AND BREAKS

INFLAMMATORY AND NON INFLAMMATORY TYPES

CAN DEVELOP KERION - OOZING ABSCESS

CONTAGION

HUMANS

ANIMALS

SOIL

SHARING BRUSHES HATS

COMMON AFRICA AND SOUTH AMERICA

GREEN FLUORESCENCE HAIRS WOODS LAMP

DOES NOT ALWAYS SHOW DUE TO INFLAMMATION

KOH OR CULTURE HAIR SHAFTS,

NIH SHAYS SCHIFF TEST- WILL ALSO SHOW GRANULOMATOUS AND NEUTROPHILLIC

TOPICAL ALONE IS NOT ENOUGH

ORAL AND TOPICAL

TOPICAL USE FOR FIRST TWO WEEKS

1% OR 2.5% SELENIUM SHAMPOO

2% MICONAZOLE

ORAL

TERBINAFINE-UP TO 6 WEEKS

FLUCONAZOLE UP TO 6 WEEKS

NIH -GRISEOFULVIN

SHOULD HAVEE NEGATIVE CUTLURE FOLLOW UP

FAMILY EDUCATION

TREAT /CHECKFAMILY

PILLOWS LINENS CLEANSE OR CHANGE

NOT SHARE BRUSHES HATS

T CORPORIS /CRURIS TOPICAL AF X 2 WEEKS

T PEDIS TOPICAL AF X 6 WEEKS OR MORE

T CAPITIS PO X 6 WEEKS OR MORE

AF SHAMPOO FOR FIRST 2 WEEKS

ONCHOMYCOSIS 48 WEEKS FOR TOPICAL

PROXIMAL SUBUNGAL ORAL ANTIFUNGALS 6-12 WEEKS

education

hygiene

shoes etc

oral therapy lft at baseline , 2 weeks then 6 weeks and prn

recheck pt prn for topical therapy

no resolution - refer to DERMATOLOGY

COMMON IN ELDERLY

CAN BE CONFUSED WITH SKIN CANCERS

SOLAR LENTIGO -LIVER OR AGE SPOTS-ARES OF FMELANIN OVERPRODUCTION

PICTURE

HEMORRHAGE IN PAPILLARY DERMIS

ON SUN EXPOSED AREAS- SKIN AND VESSELS MORE BRITTLE

ANTICOAG THERAPY

LEAVE BRONZE DISCOLORATION

BENIGN CAN BE REMOVED BY CRYOTHERAPY CURETTAGE

OR SHAVE INCISION

• SUDDEN ERUPTION OF MULTIPLE CAN MEAN INTERNAL MALIGNANCY

Impetigo is a superficial skin infection with crusting or bullae caused by streptococci, staphylococci, or both.

non bullous -clusters of vesicels or pustules with honey colored crust exudate

bullous -vesicles enlarge rapidly to become bullous

Ecthyma is an ulcerative form of impetigo. Diagnosis is clinical. Treatment is with topical and sometimes oral antibiotics

moist envrionment

poor hygiene

chronic nasopharyngeal carriage of staph or streptococci

staph predominant

mrsa common

clinical evaluation

cultures only when not responding to empiric therapy

GRAM STAIN C&S

nasal culture with recurrent

ESR

topical limited lesions

topical mupirocin ointment 3 x day for 7 days

retapamulin 2 x day for 5 days

oral therapy for 7 day regimen w agent effective against staph aureus (IDSA) unless cultures yield streptococci alone (when oral penicillin is the recommended agent)

oral abx dicloxacillin 250 qid x 7 days

cephalexin 250-500 mg qid x 10 days

AZITHROMYCIN DOSE PACK

AUGMENTIN

(erythromycin 250 mg qid po)

no empiric therapy against mrsa withou culture

idsa

MRSA doxycycline /clindamycin/smxtmp

SOAK CRUSTS WITH WET COMPRESSES TO REMOVE CRUSTS

ALLOWS PENETRATION OF TOPICAL ABX

DAILY WASHING WITH HIBICLENS

ECTHYMA

ERISYPELAS

CELLULITIS

HESV

IRRITANT DERMATITIS

LOCATION : USU HANDS

IRRITANTS: SOLVENTS , BLEACH , ALCOHOL, CHEMICALS

SYMPTOMS: BURNING PRURITIS PAIN

APPEARANCE: DRY FISSURED SKIN

LESION BORDERS: INDISTINCT

ALLERIGC

LOCATION: EXPOSED AREAS USU HANDS

CAUSE: NICKEL JEWELRY

MEDICATIONS POISON OAK OR IVY, OTHER PRODUCTS

SYMPTOMS:PRURITUS

APPEARANCE: VESICLES AND BULLAE

LESION BORDERS DISTINCT ANGLES LINE AND BORDERS

THOROUGH HISTORY

USU NO TESTS NECESSARY. ONLY IF SECONDARY INFECTION SUSPECTED

KOH

CULTURE

PATCH TEST TO IDENTIFY ALLERGEN -DERMATOLOGIST

MYCOSIS FUNGOIDES

SCABIES

PSORIASIS

SEBORRHEIC DERMATITIS

REMOVE ALLERGEN /IRRITANT

PREVENT SECONDARY INFECTION

SYMPTOM MGT

NO SCRATCHING

CALAMINE LOTION OR OATMEAL BATHS

BENADRYL 25-50 MG PO

MILD CASES HYDROCORTISONE CREAM NON RX STRENGTH 0.1 %

MID OR HIGH POTENCY

TRIAMCINOLONE 0.1 %

CLOBETASOL (HIGH) 0.05%

BARRIER CREAM - ZINC OXIDE -PROTECT SKIN AND RETAIN MOISTURE

TOPICAL _ SEVERE ITCHING , RASH DOES NOT IMPROVE 2-3 DAYS USE TOP CCS

PO

IF REACTION COVERS LARGE PORTION OF SKIN 20%, PERIORBITAL , GENITAL OR IS SEVERE

5-7 DAYS OF STEROID 0.5- 1 MG/KG /DAY , HALVE DOSE FOR NEXT 5-7 DAYS

ANTIHISTAMINES

EPIDERMIS AVASCULAR-OUTER HORNY LAYER CORNEUM ,INNER HORNY LAYER MUCOSUM, KERATINOCYTES SHED SLOUGH OFF AS SQUAMES

STRATUM CORNEUM PROTECTS AGAINT BACTERIA

INNER LAYER CONTAINS LANGERHANS CELLS -ANTIGEN PRESENTING CELLS-ALLERGIC SKIN RESPONSE AND THEY MIGRATE TO LYMPH NODES

MELANOCYTES IN BASAL EPIDERMIS PROTECT AGAINST UV

DERMIS

ECCRINE APOCRINE SEBACEOUS GLANDS FOLLICLES ETC -BLOOD SUPPLY NERVES LYMPH

EARS DERMIS HAS CERUMEN PRODUCING GLANDS

HYPODERMIS OR SUBCUTIS FAT, INSULATION, CUSHION FROM INJURY AND

The papillary dermis is the superficial layer, lying deep to the epidermis. The papillary dermis is composed of loose connective tissue that is highly vascular. The reticular layer is the deep layer, forming a thick layer of dense connective tissue that constitutes the bulk of the dermis.

OLDCARTS

PRIOR SKIN DISORDER

MEDICATIONS,OTC SCRIPT AND HERBAL, NUTRITIONAL SUPPLEMENTS

TRAVEL

SOCIAL AND OCCUPATIONAL

SELF CARE PRACTICES -LOTIONS SKIN CARE,SOAPS LLUANDRY PRODUCTS/CHANGE

FAMILY HISTORY OF ALLERGY ATOPY EXZEMA OR ASTHMA IN CHILDHOOD

CONTACT DERMATOSCOPE

OR NON CONTACT MICROSCOPE-MELANOMA

OBLIQUE LIGHT ILLUMINATE AND CONTRAST

PEN LIGHT -SYST OR PUS

WOOD LAMP -EMITS LONG WAVELENGTHS OF UV RAYS THROUGH A FILTER (>365NM) HARMLESS SHOWS ERYTHRASMA (CORNNYEBACTERIUM CORAL RED) TINEA VERSICOLOR( WHITE YELLOW), VITILIGO ( WHITE)PSEUDOMONAS PALE BLUE, DERMATOPHYTES YELLOW

FITZ PARICK - SQUEEZE SIDES AND IT INDENTS

DERMATOGRAPHISM- URTICARIA PT , RUB BACK OF FINGERNAIL -HISTAMINE RELEASED AREA BECOMES RED AND RAISED

DISTRIBUTION/LOCATION

SIZE

SHAPE

COLOR

BORDERS

SURFACE CHARACTERISTICS

DIASCOPY

USE FLAT MICROSCOPE SLIDE OR MAGNIFYING GLASS, PRESSS ON BLUE RED LESION.BLANCH FOLLOWED BY REFILL IS BLOOD IN CAPILLARIES

NO BLANCHING IS BLOOD LEACHING OUTSIDE OF CAPILLARIES EG PETECHIAE

GRAM STAIN EXUDATE - GRAM POS OR NEG

TZANCK TEST- GIANT CELLS COMMON IN HSV VZV UNROOF FRESH VESICLE

KOH -HYPHAE AND SPORES CANDIDIASIS , OR SPAGHETTI AND MEATBALLS OF TINEA VERSICOLOR ( MALASEZIA)

SCABIES

SUPERFICIAL SKIN SHAVING FROM TOP OF BURROW , OIL SOLUTION OR KOH SOLUTION

MOIST WEEPING LESIONS-BUROWS SOLUTION DRIES UP AND SOOTHES

EXUDATIVE SKIN DISEASES-WET DRESSINGS -REDUCE INFLAMMTION BY VASOCONTRICTION, PROMOTE DRYING OF LESIONS AND WOUND DEBRIDEMENT

DRY DERMATITIS

OINTMENTS

THEN CREAMS

THEN LOTIONS

THERAPEUTIC AGENTS IN OINTMENTS OR CREAMS

DONT SOAP TOO MUCH OR SHOWER TOO MUCH

PETROLATUM BIG FAVORITE BIOPSY SITES SKIN FISSURES AND IRRITATED SKIN

MEDS TOPICAL ,INTRALESIONAL, SYSTEMIC

LESIONS RX BIOPSY SURGERY ELECTROCAUTERY OR CRYOTHERAPY

REDUCE INFLAMMATORY RESPONSE

VASOCONSTRICTION

DECREASE IN COLLAGEN SYNTHESIS

NEVER USE CLASS 1-IV ON FACE OR GENITALS

CLASS 1 SUPER POTENT

CLOBETASOL PROPRIONATE 0.05%

BETAMETHASONE DIPROPRIONATE ( DIPROLENE) 0.05% OINTMENT

FLUOCINOCIDE 0.1% CREAM

CL 2 POTENT

ELOCON0.1% OINTMENT

DIPROLENE CREAM 0.05%

CL 3 UPPER MIDSTRENGTH

FKUTICASONE PROPRIONATE 0.005% OINTMENT

BETAMETHASONE VALEARATE 0.1% OINTMENT

CLASS 4 MID STRENGTH

TRIAMCINOLONE 0.1% OINTMENT/CREAM (KENALOG)

ELOCON CREAM 0.1%

CLASS 5 LOWER MID STRENGTH

FLUOCINONIDE ACETONIDE 0.025% CREAM

HYDROCORTISONE VALEARATE ( WESTCORT) 0.2 % OINTMENT

CLASS 6 MILD

DESONIDE 0.5% OINTMENT CREAM LOTION

ACLOVATE 0.05% OINT.CREAM

LEAST POTENT

HYDROCORTISONE 2.5% ,1 % , 0.5 % OIN.CRE/LOTION

COMMON WITH TCS OR THEIR VEHICLES :

CONTACT DERMATITIS

ACNE LIKE ERUPTIONS

HYPOPIGMENTATION

TOO STRONG TOO LONG AFFECTS COLLAGEN SYNTHESIS - STRIAE AND ATROPHY

TELANGIECTASIA AND PUERPERA FROM SKIN THINNING

INFLAMMATION DOWN, STOP TREATMENT, CHANGE TO LESS POTENT AGENT, OR USE INTERMITTENT RX

IF LESION WORSENS CONSIDER FUNGAL OR YEAST INFECTION

HAIRY AREAS USE FOAM SPRAY OR GEL ABSORPTION'

VEHICLES ARE BASE OF ACTIVE INGREDIENTS -CREAMS SEMISOLID EMULSIONS OF OIL IN WATER

OINTMENT IS OIL -OCCLUSIVE ENHANCE DRUG ABSORPTION

ALWAYS USE THIN LAYER

1 GM COVERS AN AREA OF 10X 10 CM

CAUSE FLARE IN PSORIASIS

AVOID DUE TO S/E

SHORT TERM TREATMENT OF SELF LIIMITED RASHES ONLY

CONTINUE PRODUCT ONE WEEK AFTER CLEARING LESION TO PREVENT RECURRENCE

TINEAS OFTEN RECUR THOUGH

SYSTEMIC ONLY FOR WIDESPREAD TINEA OR INFECTIONS THAT INVOLVE SCALP NAILS

AVOID ORAL KETOCONAZOLE HEPATOTOXICITY

TERBINAFINE NOT RECOMMENDED IF RENAL OR LIVER DX0LFFTS Q 6 WEEKS,NEUTROPENIA WITH TERBINAFINE

CREAMS POWDERS ORAL SUSPENSION,INTRAVAGINAL FOR CANDIDIASIS TABLETS LAST

ACYCLOVIR , FAMCICLOVIR VALACYLCLVIR FOR HERPETIC

CAN USE TOPICAL PENCICLOVIR ORAL HSV OR ABREVA

ACUTE FOR ORAL AV, SUPPRESS DX

SUPPRESSIVE THERAPY FOR >6 X YEAR OUTBREAKS

TNF ANTAGONISTS

BIOLOGICS/MABS

MODERATE TO SEVERE PSORIASIS

INFLIXIMAB

ETANEREPT

ADALIMUMAB

CAN BE USED FOR PSORIATIC ARTHRITIS-PRESCRIBED BY RHEUMATOLOGY OR DERMATOLOGY-SQ IM OR IVI

CAN INCREASE RISK OF LYMPHOMA, FUNGI VIRUSES MYCOBACTERIA APLASTIC ANEMIA MELANOMA AND OTHER SKIN CANCERS

PT IMMUNE STATUS AND VACCINES BEFORE STARTING MABS

5.4 million cases of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) are diagnosed each year, occurring in about 3.3 million Americans, as some people have more than one.

BASAL MOST COMMON , MELANOMA MOST FATAL

90% OF ALL SKIN CANCERS RELATED TO THE SUN

RISK FACTORS

FAIR BLUE EYES

BLONDE

FRECKLES

FAM HX

SUN EXPOSURE

HISTORY OF SUNBURN

COLOR

SUDDEN DARKENING ># TUMOR CELLS

SPREAD OF COLOR -TUMOR CELLS MIGRATING AT DIFFERENCT SPEEDS AND DIRECTIONS ( HORIZONTAL GROWTH)

RED - VASODILATION AND INFLAMMTION

BLUE - DEEPER TUMOR

WHITE INFLAMMATION OR REGRESSION

BORDER

IRREGULAR BORDERS -MIGRATION

SATELLITE PIGMENTATION -MIGRATING BEYOND CONFINES OF TUMOR

DEPIGMENTED HALO - DESTRUCTION OF MELANOCYTES ? IMMUNE? INFLAMATION

CHARACTER

SCALY

EROSION'

OOZING CRUSTING

BLEEDING

ULCERATION

ELEVATION

SYMPTOMS

PAIN

PRURITUS

TENDERNESS

TBSE INCLUDING PALMS AND SOLES,NAILS

SCALP

SUSPICIOUS LESION WARRANTS BIOPSY/REFERRAL

PEARLY BORDERS

RAISED SHINY

DEVELOP TELANGIECTASES

ADVANCED HAVE CENTRAL ULCERATION AND CRUSTING

80% OF NON MALIGNANT CANCERS

RARE TO METASTASIZE OR MORTALITY

SUN EXPOSED AREAS AS ADOLESCENT/CHILD,USU HEAD NECK ESP NOSE

TREATMENT - COMSETIC

20 % SKIN CANCERS

ACTINIC KERATOSES ARE PRE SCC

ROUGH

SUN EXPOSED AREAS STRONG COLRRELATION WITH UV

SCALY

BLEEDS EASILY

HEAPED UP APPEARANCE FROM KERATINIZATION

METASTATIC RATE 3-10%

OCCURS IN NAILS HANDS FEET OF BLACKS, BLACK SKINNED ASIANS

WHITES-BACK ANTERIOR LOWER LEGS

A ASYMMETRY

B BORDER IRREGULAR

C COLOR VARIABILITY

D DIAMETER >6MM

E ELEVATION

4% SKIIN CNACERS, 65% DEATH FROM SKIN CANCER

5 YEAR SURVIVAL RATE INVERSELY PROPORTIONAL TO DEPTH OF MELANOMA AT DIAGNOSIS

ACRAL LENTIGINOUS MELANOMA

USPSTF

INSUFFI EVIDENCE TO RECOMMEND FOR/AGAINST FULL BODY SCREENING

HCPROVIDER BE AWARE OF SKIN LESIONS WHEN PERFORMING PE

ANNUAL SCREENING FOR PTS WITH HISTORY OF SKIN CANCER

AMERICAN CANCER SOCIETY:

EVERY 3 YEARS 20-40 AND ANNUAL OVER 40 -WITH DERMATOLOGIST

EXPOSURE TO UV

FAIR, BLONDE OR RED HEAD

LIGHT BLUE OR GREEN EYES

BLISTERING SUNBURN ADOLESCENT

IMMMUNOCOMPROMISED

VERY HIGH RISK

TANNING DEVICES -INCREASE SCC2.5 FOLD

2 FIRST DEGREE RELATIVES WITH MELANOMA, 100 NEVI OR 5+ ATYPICAL NEVI

250 + TREATMENTS + UVV FOR PSORIASIS

RAD THERAPY AS CHILD

SKIN BIOPSY

SHAVE OR PUNCH OR EXCISIONAL

EACH OTHER

ACTINIC KERATOSIS-PRECNCEROUS TREAT WITH LIQUID NITROGEN

SEBORRHEIC KERATOSIS

BIOSPY EXCISIONA;

BCC ELECTRODESSICATION AND CURRETAGE

SCC TOTAL EXCISION

MM WIDE EXCISION OR MOHS

ANNUAL SKIN EXAM

ALL DIAGNOSTIC EXAMS - EXPERIENCED PROVIDER

REFER TO DERMATOLOGY FOR ALL SUSPICIOUS LESIONS

PRE CANCEROUS

ELDERLY, FAIR SKINNED SUN SENSITIVE

ROUGH SCALY SAND PAPERY, AREAS OF SUN EXPOSURE

FACE

SCALP

NECK

EARS

FOREARMS

FELT BEFORE SEEN, SANDPAPER TEXTURE

DIAGNOSIS ON PRESEENATION

BIOPSY FOR LESIONS -LOOKK LIKE SCC OR UNRESPONSIVE TO RX

20% DEVELOP INTO SCC

REFER TO DERM

LESIONS MAY REGRESS , STAY OR PROGRESS TO SCC-UNREDICATBALE

GOAL OF TREATMENT

COMPLETE ERADICATION-LIMIT PERI DAMAGE

MEDICAL

5 FU TOPICAL CREAM 5% BD X 1 MONTH

LESIONS BECOME ERYHTHEMATOUS AND HURT,ULCER AND CURST

HEAL WITHIN 2 WEEKS OF END OF TREATMENT

IMIQUIMOD TOPICAL CREAM 2-3 X DAY FOR 1 - 4 MONTHS

PHOTODYNAMIC THERAPY

ADNEXA = BIND TO, ATTACH

DERMATOLOGY IS PILOSEBACEOUS UNIT -HAIR FOLLICLE,, SEBACEOUS, ECCRINE APOCRIEN ARRECTOR PILI MUSCLE

EG SKIN HAIR NAILS

MOST COMMON DERM DISORDER IN US

DISORDER OF PILOSEBACEOUS FOLLICLES W >SEBUM PRODUCTION ALTERED KERATINIZATION, INFLAMMATION AND BACTERIAL COLONIZATION

BLACKS MORE PRONE TO POSTINFLAMMATORY HYPERPIGMENTATION

PATHO

INFLAMMATORY MEDIATORS

ABNORMAL DESQUAMATION OF KERATINOCYTES THAT PLUG THE PILOSEBACEOUS FOLLICLES

> SEBUM PRODUCTION

COLONIZE WITH PROPRIONIBACTERIUM ACNES

FACE NECK UPPER TRUNK

BLACK COMEDONES ARE OPEN FOLLICLE CELL BUILD UP

WHITE COMEDONES ARE CLOSED DD-CYSTIC SWELLING PRIOR TO BEING A PUSTULE OR PAPULE

CLINICAL EXAM

IF FANDROGEN THOUGHT TO BE PROBLEM THEN:

TOTAL TESTOSTERONE

DHEAS

LH

FSH

LIPID PROFILE

GLUCOSE TOLERANCE TESTING???

MILIA

SEBACEOUS HYPERPLASIA

DILATED PORE OF WINER ( THAT GREAT BIG BLACKHEAD)

and Favre–Racouchot syndrome LOTS OF TINY BLACKHEADS OLD MEN

MOLLUSCUM

PSUEDOFOLLICULITIS BARBAE

TOPICAL FIRST

RETINOIDS

TRETINOIN RETIN A

BENZOYL PEROXIDE

AZELEX

SALICYLIC ACID

TOPICAL ABX FOR THE P ACNES

ERYTHROMYCIN, CLINDAMYCIN, METRONIDAZOLE, NOT MONOTHERAPY

USE DWITH OTHERR TOPICALS RETINS

ORAL ABX

BENZOYL PEROXIDE ( TO REDUCE RESISTANCE)AND ERYTHROMYCIN FOR 6-8 WEEKS UP TO MONTHS

HORMONE THEAPY

ANDROGENS INDUCE ACNE

USE OCS SPIRONOLACTONE, AND DROSPIRENONE

ISOTRETINOIN - PRESCRIBED BY DERM

4-6 MONTHS

MONTHLY TRIGLYCERIDE LEVELS AND LIVER FUNCTION TESTS

TERATOGENIC

ACNE TREATMENT TAKES WEEKS TO MONTHS TO WORK - WARN THE PATINET

OFTEN COEXISTS WITH ACEN VULGARIS AND MAY MIMIC IT

AGE 30-50

WOMEN>MEN

PRIMARY DISTINCTION IS NO COMEDONES IN ROSACEA

NO CURE

TRETMENT TAKES WEEKS TO MONTHS

PATH

>SEBUM PRODUCTION

HYPERPROLIFERATION OF KERATINOCYTES, W INFLAMMATION, AND COLONISE P ACNE

FACIAL FLUSHING IS EARLY SIGN ,PROGRESSES LATER CANBE PERMANENT

FLUSH W HEAT ALCOHOL SPICY FOODS EMOTION

FLUSHING

FACIAL ERYTHEMA

INFLAMMATORY PAP AND PUSTULES

TELANGIECTASISA

WATERY IRRITATED EYES

EDEMA

PRIMARY

METRONIDAZOLE 1 % OR 0.75% GEL BID 3-4 MONTHS

AZELAIC ACID TOPICAL BID 2 MONTHS

PLEXION CLEANSER OR SULFACETAMIDE/SULFUR

ORAL ABX

TETRACYCLINE 250-500 BID OR DOXY 100-200 MG FOR 3 MONTHS

NOT RESPONSIVE TO TOPICAL OR ORAL ABX , REFER TO DERM

OCULAR FORM V SERIOUS

3 % POPULATION

EXCESSIVE SWEATING

ABNORMAL WETNESS

SWEATY PALMS

EXCESS AXILLARY SWEATING

GUSTATORY-STIMULATED SWEATING

WET SHOES

OFFENSIVE ODOR

dyshidrosis eczema

MILARIA RUBRA - FROM BLOCKED SWEAT GLANDS

IDIOPATHIC MAJORITY-SYMPATHETIC OVERSTIMULATION ECCRINE SWEAT GLANDS

2NDRY HYPERHIDROSIS IS MORE TREATABLE

LOOK FOR UNDERLYING CAUSES -PHEOCHROMOCYTOMA, DIABETES -HEAT INTOLERANCE IN UPPER HALF OF BODY AND NO SWEATING LOWER HALF IS DIABETIC PERIPHERAL AUTONOMIC NEUROPATHY

TSH R/O

THYROXINE R/O

FBG R/O DM

FSH R/O MENOPAUSE

LH R/O MENOPAUSE

IODINE STARCH TEST

URINARY CATECHOLAMINES ???

URIC ACID????

TPICAL 20% ALCOHOLIC SOLUTION OF ALUMINIUM CHLORIDE HEXAHYDRATE( DRYSOL, KERALYT)-BLOCK SWEAT DUCTS

XERAC FOR SENSITIVE SKIN

COMPLEX CARE WITH THIS, HAVE TO WEAR OCCLUSIVE WRAP

BOTOX INJECTIONS FEET, AXILLAE

THORACIC ENDOSCOPY TO INTERRUPT UPPER DORSAL SYMPATHETIC CHAIN OF D2 AND D3 CAN PROVIDE A CURE

dog bites majority- cost one billion a year

800,000 yearly visits . wmost destructive bites

occur most on children

crush

soft tissue

neurovascular

death

cat bites second most commmon 15 %

puncture

6% hospitalizattions for infection

humans -includes cfi closed fist injury

human bite sinfection rates 10%

young child

sex

self inflicted - nail bites

fight bites

>50 years

immunosuupressed (diabetic,advanced liver disese,asplenia)

crush , puncture , penetrates joint capsule or periosteum

location hand foot

failure to irrigate/debride initial management

treatment delay of >12 hours

edema at site

pvd

usu bacterial

aerobic

pasteurella including multocida

strep

staphylococci

corynebacteriium

anaerobic

bacteroides

actinomyces

porphyromonas

fusobacterium

viral

rabies,usu bats raccoons skunks foxes

tetanus

STAPH ,MRSA

STREP

EIKENELLA CORRODENS -BIG IN CFI

CAN BE RESISTANT TO EMPIRIC ABX AND CAN PRODUCE BETA LACTAMASES-

GROWS FAST CAN LEAD TO ENDOCARIDTIS

HSPITALIZATION FOR HUMAN BITES ESP OF HAND -POLYFLORA SKIN TEETH

VIRAL

RARER HSV 1 HSV 2 HEP B HEP C

HIV EXTREMELY LOW

HISTORY TAKING

LOCATION

TIME (PTS WAIT SEVEREAL DAYS)

SPECIES BEHVIOIR ANIMAL

DOMESTICATION

RABIES VACCINE STATUS

WAS ANIMAL PROVOKED

CURRENT MED LIST

PMH : EMPHASIS OM IMMUNOCOMPETENCE, SPLENECTOMY, VENOUS OR LYMPHATIC INSUFFIENCY

LIVER DX

HUMAN BITES

TEST BITER FOR INFECTIOUS DX

IS ANIMAL RABIES PRONE

PE

LOCATION, DEPTH , EXTENT, TYPE OF WOUND

S/S INFECION, INCLUDING RED STREAKING

SIGNS OF COMPARTMENT SYNDROME,SIGNS OF TENDON JOINT NERVE INVOLVEMENT

SIGNS

DISPROPORTIONATE PAIN

PARASTHESIAS

PALLOR

PARALYSIS

INFECTED WOUNDS

CBC,

ESR

CRP

AEROBIC AND ANAEROBIC CULTURES ( ANAEROBIC TRANSPORTER, NO FRIDGE,NOT FROM BOWEL OROPHARYNX, VAGINA,-AREAS OF NORMAL CIRCULATING ANAEROBES)

DEEP COMPLEX WOUNDS

X RAY STUDIES FOR BONE OR JOINT INVOLVEMENT

HUMAN BITES

HEP B

HEP C

HIV

IRRIGATE WOUND VIGILANTLY WITH AT LEAST 150 MLS STERRILE SALINE, OR WARM TAP WATER IF NONE AVAILABLE

DEVITALIZED TISSUE, FOREIGN BODIES, CLOTS CAUTIOUSLY DEBRIDED

AGGRESSIVE IRRIGATION AND DRAINAGE, WOUND PACKING NECESSARY IF CULTURES REVEAL INFECTION

MOST WOUNDS DONT DEVELOP S/S INFECTION UNTIL 24- 7 2 HOURS AFTER BITE

FACE BITES

REFER TO ED /PLASTICS IMMEDICTELY, AFTER IRRIGATION AND PREEMPTIVE ABX

DONT ATTEMPT TO CLOSE BITES -LEVEOPEN ESPECIALLY HAND, DELAYED PRIMARY OR SECONDARY CLOSURE

HAND FOOT WOUNDS IMMOBILIZED AND ELEVATED FOR 1-3 DAYS

CLOSE OUTPATIENT FOLLOW UP

FRESH UNINFECTED WOUNDS CONTROVERSY OVER ABX

CAT OR HAND BITE - 5-7 DAYS PROPHYLAXIS

SOME RECOMMEND PROPHYLACTIC ABX ALL BITES THAT PRESENT AFTER 72 HOURS

FRSH

AUGMENTIN 500/125 TID X 5-7- DAYS

CLINDAMYCIN +DOXYCYCLINE OR BACTRIM FOR PCN ALLERGY ( CLINDAMYCIN INEFFECTIVE AGAINST PASTEURELLA

LEVOFLOXACIN OR CIPRO

MACROLIDES FOR PREGANT PATIENTS ALLERGIC TO BETA LACTAMASE

OLDER INFECTED BITES = HOSPITALIZATION/ID

CAN HAVE MRSA FROM ANIMAL BITES- HIGH PREVALENCE AREAS

TMP SMX , DOXY OR CLNIDAMYCIN

SEVERE LINEZOLID PODONT USE DICLOXACILLIN CEPHALEXIN ERYTHROMYICN EMPIRICALLY AS SOLE AGENTS, NOT EFFECTIVE AGAINST PASTEURELLA OR EIKENELLA

TDAP OR TD IF FULL PRIMARY TETANUS IMMUNIZATION ( CHILD) BUT NO BOOSTER IN 5 YEARS

NO FULL SERIES- NEED TETANUS IMMUNE GLOBULIN 250- 500 UNITS IM AS FIRST OF 3 MONTHLY DOSES

RABIES

LOCATION DEPENDENT

WASH WITH 1% IODINE OR SOAP AND WATER IMMEDIATELY-LOWERS RATE ALOT

ANIMAL IS ISOLATEDOR SACRIFICED FOR BRAIN EXAM

HEAD NECK INJURY POST EXPOSURE PROPHYLAXIS

CONSIDER POST EXPOOSURE PROPH IN BITES DISTANT PAST ( CAN OCCUR 8 YEARS LATER)

RABIES IMMUNE GLOBULIN-HRIG OR PCECV -HALF INJECTED AROUND SITE , HALF IM

IMMUNIZATION ALSO 1 ML HDCV OR PCECV IM DAYS 0.3,7,14

JOINT NERVE BONE TENDON COMPARTMENT SYNDROME -ORHTO

SIGNIFCANT HAND BITES- HAND SURGEON

EXTENSIVE FOR RECONSTRUCTION, PLASTICS

HEAD INJURIES -OTOLARNYGOLOGIC OR NEUROSURGERY

SIRS,SEVERE CELLULITIS AND BITES NOT HEALING- ID

DNT HANDLE OR PROVOKE WILD ANIMALS

DONT PROVOKE DOMESTIC ANIMALS

RABIES VACCINE DOGS AND CATS MANDATROY IN US

LOOK FOR S/S RABIES- DROOLING FOAMING, FEARLESS, NERVOUS, AGGRESSIVE= RABIES

TEACH CHILDREN SAFE PET PLAY ,SUPERVISE CHILDREN

NEUTER PETS

ATOPIC

NEURODERMATITIS -KEEP SCRATCHING ,PLEASURE CENTER IN BRAIN

DYSHIDROTIC -HANDS AND TOES -IRRITANTS

SEBORRHEIC DERMATITIS -MALASEZZIA HAIR - NIZORAL ,HYDROCORTISONE FACE

STASIS DERMATITIS-( GRAVITATIONAL0-TOPICAL STEROID

NUMMULAR CHILDRENS, EXTREMITIES TRUNK, STEROID AND ABX IF OOZING ,CAN IIMITATE TINEA,TAKE SCRAPING ,USU STAPHAUREUS, MID-HIG POTENCY STEROID

CONTACT DERMATITIS

HISTORY OF ASTHMA OR ALLERGIC RHINITIS

FLEXURAL INVOLVEMENT

HISTORY OF GENERALIZED DRY SKIN

ONSET OF RASH BEFORE TWO YEARS OF AGE

ALLEVIATE PRURITUS

DECREASE DRYNESS AND INFLAMMATION

PREVENT INFECTION

TEPID BATH/SOAK FOR FLARE UPS

NO VERY HOT WATER , LIMIT BATHING

SUPERFATTED SOAPS

EMOLLIENTS: EUCERIN, CETAPHIL, AQUAPHOR -GREASY, CERA VE

PRURITUS

ATARAX 25 MG TID, QID

BENADRYL 25-50 4-6HOURLY MAX 300 MG /24 HOURS

NON DROWSY

XYSAL

LORATADINE-CLARITIN

INFLAMMATION

TOPICAL STEROIDS

HYDROCORTISONE

FLUTICASONE PROPRIONATE CUTIVATE CREAM 0.05%

DC WHEN INFLAMMATION SUBSIDES , EMOLLIENT SHOULD BE CONTINUED

POTENCY DEPENDS ON LOCATION AND PRESENTATION

NON STEROIDAL CALCINEURIN INHIBITOR

INDICATORS:MOD-SEVERE ECZEMA, CONCERN OF TCS S/E

USE IS SHORT TERM INTERMITTENT

TACROLIMUS 0.03% AND 0.1%

pimecrolimus cream.ELIDEL 1%

MAINTENANCE 2/WEEK X 12 MONTHS

INTERMITTENT ATOPY 1-2 X ANNUAL

USE IM CCS OR OCS

TYPICAL DOSE PACK IS INSUFFICENT -USU REQUIRES 2-3 WEEKS

TAPER OCS 60/40/20 OVER 15-21 DAYS

FF/U 2 WEEKS AND 6-8 WEEKS

IF SEVERE FLARE UP INCREASE POTENCY X 2 WEEKS

MOISTURIZE

AVOID/TREAT SECONDARY INFECTION

ECZEMA PATIENTS MORE PRONE TO HERPES, MOLLUSCUM WARTS

SERIOUS VIRAL COMPLICATION IS EH

PT USUALLY HAS UNDERLYING SKIN DISORDER USU AD AND DEVELOPS WIDESPREAD ERUPTION OF VESICLES AND EROSIONS WHEN EXPERIENCING PRIMARY HERPES OR HERPES REACTIVATION

DIAGNOSED WITH GIEMSA STAINED SCRAPING-MULTINUCLEATED GIANT CELLS- TZANK SMEAR I THINK

TREATMENT

ORAL ANTIVIRAL EG VALTREX

CHRONIC INFLAMMATION TISSUE SURROUNDING NAIL

BACTERIAL OR FUNGAL

OR NON INFECTIOUS:

CHEMICAL IRRITANTS

WATER

vzv downregulates mhc and enables virus to evade immune response

prolonged incubation period

moves retrograde along sensory axons, establishes life long latency in regional ganglia ( reservoir)

reactivates -causes intense inflammation

and hemorrhagic necrosis of nerve endingss-typical neuropathic pain

neuronal loss of ganglion and fibrosis of afferent nerve fibers esp type c nociceptors

AGE

IMMUNE STATUS-ANTIVRALS USED FOR TRANSPLANT RECIPIENTS

BIOLOGICS INCREASED RISK OF HZVHIV

WOMEN

WHITES

CAN TRANSMIT VZV TO VARICELLA NAIVE PTS

DISSEMINATED HZV IS AIRBORNE PRECAUTIONS

ERYTHEMATOUS PAPULES

SINGLE DERMATOME

OR SEVERAL CONTIGUOUS DERMATOMES USU THORACIC AND LUMBAR, EYES - ANYWHERE

GROUPED VESICLES OR BULLAE AFTER FEW DAYS

3-4 DAYS LATER -PUSTULES

CAN BECOME HEMORRHAGIC

PRODROMAL PAIN PRECEDES RASH BY TWO TO THREE DAYS

POST HERPETIC NEURALGIA 90 DAYS UP TO YEAR 3/10 OR MORE

PARASTHESIAS PRURITUS ALLODYNIA IN AFFECTED DERMATOME

10-15% DEVELOP PHN

HERPES ZOSTER OPTHALMICUS

SIGHT THREATENING CONFDITION

PRODROME HEADACHE MALAISE FEVER

HYPERREMIC CONJUUNCTIVITS,EPISCLERITIS KERATITIS-STRONGEST FOR VISION LOSS

IF ON NOSE DEFINITE EYE INVOLVEMENT

ACUTE RETINAL NECROSIS

5TH CRANIAL NERVE

RAMSAY HUNT SYNDROME

IPSILATERAL FACIAL PARALYSIS EAR PAIN VESICLE IN AURICLE OR CANAL-8TH CRANIAL NERVE

OTHER RARER CONDITIONS

CLINICAL PRESENTATION

PCR ONLY IF UNSURE OF DIAGNOSIS

CAN DO PCR WITH CRUSTS EVEN, AND VITREOUS HUMOR

HIV TESTING IN AT RISK POPULATIONS

RECURRENT HZV RARER

WOMEN > MEN

ANTIVIRALS

VALACYCLOVIR PRODRUG 1000 MG TID X 7 DAYS

FAMCICLOVIR PRODRUG 500 MD TID X 7 DAYS MORE EXPENSIVE

ACYCLOVIR LOWER BIOAVAILABLITY 800 MG 5 X DAY X 7 DAYS LOWER COMPLIANCE

BETTER RECOVERY WITHIN 72 HOURS FROM RASH ONSET

PREGNANCY

UPTODATE PREFERS ACYCLOVIR AS LONGEST HISTORY

ANALGESIA

CORTICOSTEROIDS

PREDNISONE 14-21 DAYS TAPER 40 MG AS START

NSAID

SHORT ACTING OPIODS OXYCODONE 5 MG (utd)

GABAPENTIN CANBE USED

LIDOCAINE 4% Q 6 HOURLY ( sHADOWHEALTH)

ISOLATE TILL CRUSTS OVER

WASH TOWELS SHEET

DONT SCRATCH AS HEAL

LOOSE FITTING COTTON CLOTHING

ANAPLASMOSIS BLACKLEGGED ICK NORTH EAST REGION IXODES SCAPULARIS

BABESIOSIS PARAPSIES INFECTE RED BLOOD CELLS BABESIA MICROTI

THERE ARE OTHER TICK DISEASES NOT IN NORTHEAST

BORRELIA MAYONII MID WEST CAUSES LYME

BORELLIA BURGDORFEIR AND IXODES SCAPULARIS IN NE US CAUSE LYME DISEASE

BALCK LEGGED TICKS LYME IS A SPIROCHETE BACTERIA

FEVER

HEADACHE

FATIGUE

REGIONAL LYMPHADENOPATHY

SKIN RASH ERYTHEMA MIGRANS 80% OF PATEITNS

UNTREATED SPREADS TO JOINTS HEART AND NERVOUS SYSTEM

DIAGNOSIS

IMPACTED BY PREVIOUS INFECTION

TRADITIONAL:

ELISA TEST,- IGM + IGG ,MAY BE CROSS REACTIONS , FALSE + IGM MORE COMMON IF POSITIVE THEN WESTERN BLOT ASSAY

WESTERN BLOT ASSAY HAS SEPARATE IGM AND IGG BLOTS

IGM + IF 2 OR 3 BANDS DETECTED

IGG + IF 5 OR 10 BANDS DETECTED

WESTERN BLOT GM PRONE TO FALSE POSITIVES (UTD)

SOMETIMES PROPHYLAXIS AFTER TICK BITE

SINGLE EM JIS TREATED DIFFERENTLY TO MULTIPLE E/ MIGRANS WHICH IS EARLY DISSEMINATED DISEASE

ALL PTS WITH EM SHOUED BE TREATED EARLY

1.DOXYCYCLINE100 MG PO BID X 10 DAYS

AMOXICILLIN 500 MG PO TID X 14 DAYS

CEFUROXIME 500 MG BID x 14 DAYS

BACTRIM

DOXYCYLINE 100 BID X5-10 DAYS

CLINDAMYCIN 300-450 BID X 5-7 DAYS

BECOMES APPARENT INI SUMMER WHEN PT TANS J

AFFECTED AREAS DO NOT TAN

APPEAR ON CHEST AND BACK

TREAT WITH ORAL ANTIFUNGAL AGENT OR TOPICAL SELENIUM SULFIDE