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MACULOPAPU LAR RED RASH Viral exanthem NOS Rubeola Rubella Roseola Erythema Infectiosum Scarlet Fever RockyMtn Spotted F Hand-foot-mouth Kawasaki's disesase Drug eruption Staph scalded skin Staph toxic shock Strep toxic shock Erythema Multiforme Steven's Johnson Psoriasis Urticaria Pityriasis Rosea Disseminated gonorr Scabies

MACULOPAPU LAR RED AND SCALY RASH +/- Patches and Placques Pityriasis Rosea Atopic Dermatitis Contact Dermatitis Seborrheic dermatitis Tinea capitis Tinea corporis Tinea pedis Tinea versicolor Lichen plannus

VESICULAR/ BULLOUS Herpes simplex Varicella Herpes zoster Pemphigus Pemphigoid Bullous impetigo Staph Scalded Skin Epidermolysis bullosa TEN

PETECHIAL RASH/ PURPURIC RASH Vascular Integrity -Trauma: NAT, etc -Vasculitis: HSP,etc -Drugs -Infections: viral, mono, ricketsia, strep, endocarditis Platelet disorder -ITP -TTP -HUS -SEPSIS/DIC Meningococcus,et c -Drug induced -BM infiltration -Liver failure -Congenital plt d/o Coagulation disorder -Congential: VWD, hemophilia A,B -Acquired: DIC, warfarin, Vit K deficient, liver dz, renal dz

PAPULAR OR NODULAR RASH Pediculosis Scabies Molluscum Syphillus Warts Xanthomas Insect Bites Milia Mastocytomas Contact dermatitis Erythema Nodosum Erythema Multiforme

PUSTULAR Impetigo Folliculitis Carbuncle Hiradenitis Suppurati Gonococcal dermatitis

DIFFERENTIAL DIAGNOSIS OF A RASH IN A TOXIC PATIENT Steven's Johnson syndrome Staphylococcal toxic shock syndrome Staphylococcal scalded skin syndrome Streptococcal toxic shock syndrome Pemphigus/Pemphigoid Kawasaki's syndrome Vasculitis Drug reaction Rocky Mountain Spotted Fever GENERAL NOTES Macular = red/pink color change < 0.5cm Patch = color change > 0.5 cm Papular = raised lesion Nodule = round elevated lesion > 0.5cm Plaque = elevated lesion >0.5 cm Finish definitions Approach to diagnosis Is the person toxic? Is the rash maculopapular, scaly, papular, nodular, vesicular, bullous, pustular, petechial or purpuric? Are there any recongnizable features of the rash or history? Is the rash acute or chronic? Is the rash associated with fever or infectious symptoms? Is the rash localized to an area of contact? Is the rash scaly? Common precipitants: drugs, infections, food,

THE RED MACULOPAPULAR RASH +/- SCALES SCALES, PLAQUES, PATCHES FUNGAL INFECTIONS Principles Dermatophytoses = superficial fungal infections that are limited to skin Scaling, papules, plaques and patches are most common Grow best in heat and moistoure Only grow in keratin or outer layer of skink, nails, hair

Keratin accumulates in body folds Not very contagious (except Tinea capitis) KOH preparation: branching hyphae of the dermatophytes or the short, thick hyphae and clustered spores of tinea versicolor. Cultures of hair, nail, scales using Saboranund agar X 3 weeks Tinea Capitis Clinical Features Fungal infection of the scalp MC in preschoolers but increasingly common in adults etc More common in african americans Trichophyton tonsurans is cause of current epidemic (many have seborrheic-like scaling in the abscence of alopecia) Black dots representing hair broken off near the scalp Hair loss occurs b/c hyphae grow within the shaft thus the shaft is fragile and breaks off 1-2 mm from the scalp Circular patches of baldness may result Close personal contact spread Secondary bacterial infection as a complication Diagnosis and Differential Considerations Ddx of tinea capitis: alopecia areata, atopic dermatitis, nummular eczema, bacterial infections, apsoriasis, seborrheic dermaitits, tinea amiantacea, trichotillomania (hair pulling), histiocytosis KOH prep is not helpful; fungal culture should be obtained Bacterial culture if you think there is bacterial superinfection Management Griseofulvin 20 mg/kg od x 6 weeks (or fluconazole) Systemic therapy is required Refer for follow up and family should be evaluated Selenium sulfide shampooo 250 mg 2x/week decreases shedding Kerion Dermatophytic infection of the scalp that appears as an indurated, boggy inflammatory plaque studded with pustules Usually mistaken for bacterial infection Treat with Griseofulvin + prednisone for 2 weeks (decreases inflammation and scarring) Add keflex or clox if added bacterial infection occurs Tinea Corporis Classic "ring-worm" infection Arms, legs, trunk Sharply marginated, annular lesion with raised or vesicular margins and central clearing Single, multiple, or concentric lesions Tinea cruris:involves the groin, perineum, thighs, buttock (note that the scrotum is characteristically spared) Ddx: granuloma annular psoriasis, erythrasma, intertigo with secondary candidiasis Usually respond to topical therapy alone Many effective topical antifungal agents: Lotrimin, Tinactin, Micatin, terbinafine, griseofulvin, naftifine, etc

Apply to affected area tid X 2-3 weeks or until resolution Acute inflammatory blistering lesions: wet compresses of Burow's solution: aluminum acetate solution that is useful for oozing, wet inflammatory lesions\

Tinea Pedis Athlete's foot Scaling, maceration, vesiculation, fissuring between the toes and on the plantar surface of the foot Entire sole may be involved Secondary bacterial infections can occur Vesicular pustular form of tinea pedis should be considered with vesicles or pustules on inner aspect of foot Ddx: contact dermatitis and dyshidrotic eczema KOH prep helps differentiate Treatment: topical antifungal preparation until cleared (see above) Tinea Versicolor Superficial yeast infection caused by Pityrosporum ovale Superficial scaling patches occur mainly on the chest and trunk but may extend to the head and limbs Lesions are colorful: pink, tan, white May be itchy; patient may complain that the spots won't tan Fine subtle scale is noted that may appear hypopigmented Pale yellow or orange florescence with Wood's light Ddx: vitiligo, seborrheic dermatitis KOH prep: short hyphae mixed with spores (spagetti and meatballs) Mx: 2.5% selenium sulfide shampoo, imidazole creams or oral ketoconazole as a singel 400 mg dose or 200 mg po od X 5 days Recurrence rates are 30% Monthly prophylaxsis with selenium shampoos Tinea Unguium Fungal nail infection = opaque, thickened, cracked, crumbled nails Subungual debris; nail may have longitudingal yellow streaks Nail of great toe is MC location Mx: topical therapy rarely effective: Fluconazole, itraconazole, terbinafine are all acceptable options Recurrence common, may require nail removal

CANDIDIASIS Perspective Infections more common in young, elderly, immunocompromised, diabetics, chronic steriods, endocrine disorders, cancers, antibiotics Oral Thrush

MC candidal infection MC in newborns Patches of white gray friable material covering an erythematous base on the buccal mucosa, gingiva, tongue, palate, or tonsils Fissures or crust at the corners of the mouth may be present AIDS defining illness Consider immunosuppression in abscence of abx use or dentures Dx is lichen planus (not easily scraped off as candida is) Mx Oral nystatin suspension (100,000 units/ml) qid Infants: 1ml painting the mouth qid Older children and adults: 4-6ml swish and swallow qid Treat for 7/7 or until lesions dissapear Clotrimazole troches dissolved in the mouth qid is an option in adults Oral ketoconazole or fluconazole is an option (some think this is the way to go) Soak dentures in sodium hypochlorite 1:10 solution at night

Cutaneous Candidiasis Moist, warm areas of groin, axilla, folds, etc Moist lesions, bright-red macules rimmed witha collarette of scale which represents the pustule roof with scalloped borders Small satellite papules or pustules are just peripheral to the main rash Satellite lesions are the most typical indicators of candidiasis Intertirginous lesions prone to bacterial superinfection Candidal onychia and paronychia: hands frequently in hot water, thumb sucking Ddx: contact dermatitis, tinea cruris, intertrigo, malaria, folliculitis Candiasis: less sharply demarcated than tinea cruris and brighter red than intertrigo KOH prep from pustule and roof of the lesion will reveal hyphae and pseudohyphae Mx Clean mucky areas and expose to air (fan etc) Wet compresses with Burow's solution for inflammatory lesion Imidazole cream to affected area qid (ketoconaloze, clotrimazole, miconazloe, econazole) Candidal paryonychia: protect hands from water, nystatin or clotrimazole cream to nail for for 8 weeks

PITYRIASIS ROSEA Mild skin eruption predominantly found in children and young adults Lesions are pink or pigmented oval papules or plaques 1-2 cm Primarily on the trunk and proximal extremities Mild scaling may be present Lesions are parallel to the ribs, form ing a Christmas tree-like distribution on the trunk Oral lesions are rare Papular or vesicular lesion variants occur in kids Herald Patch preceeds generalized eruption by one week in 50%

Herald Patch is a large 2-6cm patch Usually asymptomatic but may be mildly pruritic Self limited, resolves w/i weeks Viral cause suspected Ddx: tinea corporis, guttate psoriasis, lichen planus, drug eruption, secondary syphillus Recurrence rate Treatment only symptomatic for pruritis if present

Eczema = dermatitis (constellation of disorders that include erythema, edema, vesiculation, scaling, pruritis) ATOPIC DERMATITIS Principles Cutaneous manifestation of atopic state Not an allergic disorder in itself Is associated with allergic disorders: asthma, allergic rhinitis Abnormalities of humoral and cell-mediated immunity Eosinophils, mast cells, and lymphocyte activation triggered by increased production of interleukin 4 by T-helper cells seems to be involved Increased IgE levels found in most but not all and levels do not correlate Course is remissions and exacerbations Clinical Features Inflammatory, thickened, papular or paulovesicluar lichenification May show hyperpigmentation of the skin Skin is typically dry and may be scaly Skin also can be vesicular, wet, weeping, oozing in the acute phase Infants: cheeks, extensor surfaces, diaper area Older children: antecubital and popliteal flexion areas, neck/face/chest Infantile atopic dermatitis usually begins at 4-6 months and imporves by 4-6yrs Childhood form: begins at a4-6 years and resolves or continues into adulthood INTENSE PRURTITIS is the hallmark of atopic dermatitis Itching can be focal or generalized, worse in the winter, triggered by increased body temp and stress, worse at night, excoriations common from scratching Secondary bacterial infection is common Repeat scratching and rubbing leads to lichenification (hyperpigmented, thick skin with accentuation of skin furrows) Differential Considerations Ddx: histiocytosis X, wiskott-aldrich syndrome, chronic seborrheic dermatitis, phenylkeotonuria, bruton's x-linked agammaglobulinemias, psoriasis, scabies, drug eruption, contact dermatitis Complications: bacterial infection, otitis externa, cataracts, keratoconus, retinal detachment, cutaneous viral infections

Management Goals: control inflammation, dryness, itching Vaseline or Eucerin cream 10% (not lotion) to reduce dryness Exudative areas: apply wet dressing of gauze soaked in Burow's solution; apply for 20 minutes qid Antihistamines Systemic steroids for very severe Cyclosporin, Ultraviolet B treatment, and other immunosuppressive are options for very severe disease Topical corticosteroids ointments are mainstay of treatment Mild disease: less concentrated ointment Face: triamcinolone 0.025% (milder) used b/c strong steroids can cause permanent cutaneous atrophy on the face Severe disease: florinated corticosteroid ointment (1/2 strength betamethasone valerate) to affected areas tid FIRST LINE TREATMENTS OF ECZEMA Antihistamines: gravol, benadryl, atarax Aveeno baths Bactroban ointment Celestoderm George's cream Oatmeal baths Corticosteroid ointments SECOND LINE THERAPIES Protopic (Tacrolimus) Cyclosporine Prednisone Oral antibiotics RED MACULES DRUG ERUPTION Principles Different eruption of same drug in different individuals MC eruptions are urticarial and morbilliform rashes Tend to appear within a week after drug is taken (not necessarily right away) Reactions to semisynthetic penicillins tends to occur later May appear after drug has been discontinued Atopic patients with asthma, hay fever, eczema are at increased risk RARELY produce reactions: acetaminophen, codeine, digoxin, erythromycin, demerol, morphine, prednisone, maalox Clinical Features (see table 114-2) Exanthems: resemble viral and bacterial infections, usually widespread symmetric maculopapular eruptions

Eczematous drug rashes: resemble contact dermatitis but are more extensive; begin as erythematous or papular eruptions and become vesicular; prior sensitization is common with this type of reaction Vasculitis lesions: begin as erythematous papules or nodules but may ulcerate and become gangrenous. Purpuric drug eruptions may be the result of bone marrow supression, vasculitis, or platelet destruction. Platelet transfusion, plasmapharesis, steroids, splenectomy in severe cases Photosensitive druge reactions: require sunlight Phototoxic: more common; sulfa drugs/thiazides/tetracycline are common causes, not immunologic and can occur in any person; look like a sunburn but may have bullous or papular features; pruritis is minimal or absent Photoallergic: the result of antigen formation that results in sensitized lymphocytes (delayed immunoloci response); only occurs in sensitized individuals, usually 2 weeks after exposure to the drug and sunlight; not dose related, usually look eczematous and is intensely pruritic; chlorpromazine/promethazine/chlordiazepoxide are common sensitizers of photoallergic reactions; d/c drug and avoid sunlight/use sunscreen Fixed drug eruptions: appear and recur at the same anatomic site after repeateed exposures; sharply marginated and round/oval; may be pigmented, erythematous, or violaceous; may be pruritic Ddx Viral examthem, chronic exfoliative erythroderma: caused by psoriasis or eczema, sScarlet fever, Staphylococcal scarliatiniform eruption, Kawasaki's syndrome Management D/c drug Warn that resolution will be slow Calamine lotion, cool compresses, tepid water baths with colloidal oatmeal (Aveeno) or cornstarch, antihistamines

STAPHLOCOCCAL SCALDED SKIN Generally occurs in children < 6yo Erythema and crusting around the mouth Erythema then spreads to the body Bullae form and the skin desquamates Also called Stapylococcal Epidermal necrolysis Exfoliative toxin produced by phage groupt II, type 71 Stapylococci Toxin acts at the zona granulosa of skin to produce a superficial separation that results in widespread painful erythema, blisters Usually occurs in children 6 mo to 6 yrs Mortality 3% in kids but 50% in aldults and near 100% in adults with comorbidities Mucous membranes SPRARED (can have mild inflammation but not involved to the extent of Toxic Epidermal Necrolysis) Nikolski's sign = the easy separation of the outer portion of the epidermis form the basal layer when pressure is exerted; often but not always present Vesicles and bullae are characteristic Loss of large sheet of superficial epidermis ----> Looks like SCALDED SKIN

Main ddx is Toxic Epidermal Necrolysis (TEN): usually cause by medications, mucous membranes are INVOLVED Dx can be confirmed by biopsy or frozen section demonstrating subglandular epithelial separation Lesions dry up after desquamation and resolution within 7 days Mx Most group 2 are penicillinase resistant Most recover without abx Naficillin, cloxacillin, dicloxacillin recomended TOXIC SHOCK SYNDROMES TSS = acute febrile illness characterized by diffuse desquamating erythroderma High fever, hypotension, constitutional symptoms, MSOF, rash Exotoxin-procuding S.aureus Post op setting is most common outside of tampon related Also associated with various staph/strep infections: cellulitis, erisepalis, PTA, sinusitis, burns, septic abortion, skin abscesses Stapylococcal and Streptococcal toxic shock syndromes STAPHYLOCOCCAL TOXIC SHOCK SYNDROME Perspective Often occurs in females related to tampons Incidence has decreased remarkable since high - absorbent tampons sere withdrawn from the market Now most cases related to focal soft tissue infections with staph Pathophys and Clinical Features Staph aureus isolated in 90% of cases related to tampons Results from TOXIN FROM PHAGE GROUP 1 S. aureus Fever, "sunburn" or sandpaper rash, hypotension, tackycardia and at least three organ system involvement Mucosal inflammation, myalgia, profuse watery diarrhea, mental status changes are common Differential diagnosis: streptococcal scarlet fever, stretococcal toxic shock syndrome, rocky mountain spotted fever, kawasaki syndrome, leptospirosis Managment Fluid resuscitation Vasopressors/ionotropes: need alpha and beta adrenergics IV antibiotics to cover penicillinase-producing staph: clox, naficillin, etc Clindamycin and vancomycin options for pen allergic Remove tampon Remove foreign bodies Drain abscesses Systemic steroids if given early may help CRITERIA FOR DIAGNOSIS (SSSTT) Skin Rash (diffuse macular erythema): sunburn or sandpaper looking ­> resembles scarlet fever Skin Desquamation 1-2 weeks after onset SBP < 90 or orthostatic drop + symptoms Temp > 38.9 Three organ systems (clinical or lab)

GI: N/V/D MSK: myalgias, CK doubled Mucous membranes: vaginal, oral, conjunctival Renal: BUN or Scr doubled or pyuria > 5 cells/hpf Hepatic: bili , AST/ALT doubled Hem: platelets < 100 Neuro: altered LOC with no focality

STREPTOCOCCAL TOXIC SHOCK SYNDROME (STSS) Perspective Described in 1987 Predominantly caused by group A strains but can be caused by other groups Pathophysiology and Clinical features Predisposing factors: surgery, minor trauma, hematomas, muscle strain,m cellulitis, chicken pox; Mortality 30% MOST common cause in children is strep superinfection of chicken pos lesion Association with NSAID use which may mask presenting symptoms resulting in increased severity of disease Severe pain, abrupt onset Pain often present before physical findings Usually in extremities but may be pelvic, abdominal, chest, etc Minority have influenza like symptoms FEVER is the most common sign (can be hypothermic if sick) Tachycardia, hypotnesion, soft tissue infection signs, scarlet - fever like rash (sandpaper) are all common Renal failure, respiratory failure, DIC, MSOF, shock (septic and cardiogenic from cardiotoxic effects) are all complications NOTE: shock is predominantly cardiogenic: LOW CO and high SVR Streptococcal M and T serotypes Due to exotoxin A and B: toxins act as superantigens to activate T cells resulting in MASSIVE release of inflammatory mediators; fever, rash, hypotension, and MSOF Ddx: staph toxic shock, grm -ve sepsis, endotoxic shock Diagnosis Scr increase; Consider deeper infection if CK up Labs may show DIC; Blood cultures positive in 60%; Wound cultures positive in 95% DIAGNOSTIC CRITERIA (must meet both) Isolation of Group A strep From a normally sterile site (blood, CSF) is a definitive case From a normally non-sterile (sputum, skin) is a probable case Hypotension + at least two of.... Renal failure Coagulopathy Liver involvement

ARDS Generalized macular rash (may desquamate) Soft tissue necrosis Management Supportive, usually ICU Initial abx needs to cover staph and strep b/c hard to distinguish Penicillin + clindamycin Ceftriaxone + clindamycin Penicillin not great against a large inoculum with nec. fasc. Clindamycin advantages: not effected by large inoculum, kills cell wall-deficient streptococci, long post administration efficacy, enhances opsonization of streptococcal organisms when grown with low concentrations of penicillin Surgical consult for early surgical debridement IV gamma globulin may help: has antibodies against staphylococcal toxins which may cross react with streptococcal toxins Steroids: case reports indicate there may be benefit of dexamethasone if given with gamma globulin Antibiotic prophylaxis NOT recommended for household contacts

TOXIC EPIDERMAL NECROLYSIS Principles Non-staphylococcal induced toxic epidermal necrolysis Hallmark = separation of large sheets of epidermis from underlying dermis Full thickness of epidermis is involved Skin biopsy easily distinguishes b/w TEN and staphylococcal scalded skin Moratility 20% Rarely associated with vaccinations (polio, measles, smallpox, td) Drugs Penicillin Sulpha Tegretol NSAIDs Allopurinol Barbituates Clinical Features Mucosal lesion common; may precede exanthem Nikolski's sign: rubbing results in desquamation of underlying skin including the pigment (staph scalded skin ----> pigment remains) Onset: face and mucous membranes Ocular involvement can occur Erythema usually precedes the loosening of the epidermis Management D/c drug Fluid replacement as per burn Control infection Steroids controversial

Plasmapharesis experimental MAINSTAY of managment is wound care and prevention of secondary bacterial infection ------> should be managed in burn center ERYTHEMA MULTIFORME Etiology Drugs and HSV infections are the MCC Viral infections (heptitis, influenza) are next MCC Fungal infections: dermatophytosis, histoplasmosis, cocidiomyocosis Bacterial infections: strep and TB Collagen vascular disorders: RA, SLE, dermatomyositis, PAN Cancers Pregnancy DDX Urticaria Scalded skin syndrome Pemphigus Pemphigoid Viral exanthems Clinical Features Acute, self-limiting disease Erythematous or violaceous macules, papules, vesicles, or bullae Symmetrical distribution common Most common in PALMS and SOLES, back of hands or feet, extensor surfaces of the extremities Target Lesion with three zones of color is the hallmark: centra dark papule or vesicle, surrounded by a pale zone, a halo of erythema Steven - Johnson Syndrome = Toxic Exctodermal Necrolysis Severe form of EM Bullae, mucous membrane lesions, MSOF Chills, malaise, headache, fever, tachycardia, hypotension Purulent conjunctivitis may occur and be severe Management Look for underlying etiology Resolve spontaneously in 2-3 weeks in mild forms Severe cases: admit, iv hydration, burn unit care, systemic analgesia, systemic corticosteroids Wet compresses with dressing soaked in 1:16000 solution of potassium permanganate or 0.05% silver nitrate several times a day to bullous lesions Look for infection and hypovolemia

URTICARIA Principles 20% will eventually get urticaria Acute and chronic forms Chronic urticaria more common in women Histamine, bradykinin, kallikrein, acethycholine as mediatesors Immunologic reaction: anaphylaxis, serum sickness Nonimmunologic reaction: degranulation of mast cell by foods, drugs

Contact urticari: foods, textiles, animal dander and saliva, plants, topical medications, cosmetics, chemical Any drug can cause urticaria: penicillin and aspirin are most common Any food can cause urticaria: food allergy (fish, nuts, eggs) or non-immunologic histamine release (holbster, strawberries) Hereditary urticaria and angioneurotic edema exist Infections: common cause in children, less common in adults; hepatitis, mono, coxsackie more commonly produce urticaria Inhalation: pollens, mold, animal dander, dust, plant materials Stings and bites Other associations: SLE, lymphoma, carcinoma, rheumatic fever, hyperthyroid, JRA Dermatographism: urticarial wheal within 30 minutes after pressure Pressure urticaria: urticarial wheal forms 4-8 hours after pressure Cold urticaria: familial or acquired; associated with cryoglobulinemai, cryofibrogenemia, syphillus, connective tissue disorders: suppression with cyproheptadine 4mg tid, antihistamines before cold exposure; doxepin qhs Cholinergic urticaria: induced by heat, exercise, or stress; wheals of 1-2 mm surrounded by erythematous flares and occassionally satellite wheals; responds to hydroxyzine Heat and solar urticaria uncommon Chronic urticaria etiology often unknown

DDX OF URTICARIA F Foods P Plants A Animals D Drugs I Infections C Contacts (cosmetics,etc) O Other:cold, cholinergic, chronic P Physical: dermatograph, pressure

Clinical Features Edematous plaques with pale centers and red borders Individual hives are transient (lasting < 24hrs) New hives may continually develop Ddx: erythema multiforme, erythema marginatum (R.F.), erythema migrans (Lyme dz), JRA Management Remove inciting factor if possible H1 antagonists: benadryl, gravol, Hydroxyzine (Atarax, Vistaril): 10 - 25 mg (2 mg/kg/24hr in kids); supposed to be less sedating than benadryl, gravol H2 antagonists: actually good for skin, ranitidine/cimetidine Fexofenadine, astemizole, terfenadine are supposed to be even less sedating Prednisone X few days: effective utricaria can rebound after discontinuation When to use prednisone? Failed treatment with antihistamines, severe symptoms, anaphylaxisis

EXANTHEMS PRINCIPLES OF EXANTHEMS Exanthem = skin eruption that occurs as a symptom of a generalized disease Known infectious causes: 30+ enteroviruses (mostly coxsacki and echoviruses) as well as adenovirus have a particular nack to cause exanthems Most are maculopapular although scarlatiniform, erythematous, vesicular, and petechial rashes Usually nonpuritis, do not desquamate, and vary in extent Mucous membrane lesions may occur Echovirus type 9: meningitis, petechial exanthem resembling meningococcemia Echovirus type 16 (Boston exanthem): may resemble roseola Coxsackie group B type 5 may also resemble roseola in adults Coxsackie group A type 16: distinctive syndrome of vesicular stomatitis, oral vesicles, dorsum of hands and lateral borders of feet; may be associated with meningoencephalitis Classic viral exanthems Roseola Infantum = Exanthem subitum (HHV6) Rubella (German measles) Rubeola (measles) Erythema infectiosum = fifth disease (parvovirus B19) Enteroviruses: coxsackie, echo MEASLES (RUBEOLA) Clinical Features Highly contagious virus; droplet spread; incubation 10 days Now usually only seen in nonimmunized, immigrants Contagious from 2 days before symptoms until 4 days after rash appears Fever, malaise mark onset of symptoms; coryza, conjunctivitis, and cough begin within 24hours of the onset of symptoms Fever increases daily in a stepwise fashion until it reaches approximately 40.5 degrees celcius on the 4th - 5th day Koplick's spots are pathognomonic: small, irregular, bright red spots with bluish-white centers that begin opposite the molars then spread to the adjacent oropharynx; usually appear on second day of illness Cutaneous eruption begins on th 3rd - 5th day of illness (rash BEFORE defervescence) Maculopapular erythematous lesions involve the forehead and upper neck then spread to the face, trunk, arms, and finally the feet (SPREADS TOP DOWN) Koplick's spots disappear as the rash appears The rash begins to fade in the order of appearance (starts on 3rd day) Complications: OM (most common), encephalitis (1 in 1000), pneumonitis Management Antibiotics indicated for bacterial superinfections (OM, etc) only Supportive treatment only Isolation of limited value b/c not infectious by the time it is diagnosed Human immune globulin in a susceptible person within 6 days of exposure (0.25 ml/kg IM in children). Live virus vaccine given w/i 72 hrs of exposure may be effective in prevention Vitamin A shortly after exposures?? ? indications for immune globulin

ROSEOLA INFANTUM = EXANTHEM SUBITUM = SIXTH DISEASE Caused by Human Herpes Virus 6 Fever and skin eruption 95% occur in 6mo to 3yrs and most are < 2yo Febrile seizures may occur Abrupt onset fever, rising rapidly to 40 degreees Temperature continues for 3-4 days (constant or fluctuant) then rapidly decreases to normal Rash appears with defervescence Pink or rose colored macules or maculopapules 2-3 mm diameter which blanch on pressure and rarely coalesce; trunk initially the SPREAD PERIPHERALLY to neck and extremities Rash clears over 1-2 days without desquamation LOOKS WELL despite high fever Encephalitis rare, very few complications Excellent prognosis, no treatment

RUBELLA = GERMAN MEASLES Fever, skin eruption, generalized lymphadenopathy Spread by droplet contact; peak in winter and spring Incubation 14 - 21 days: contagious few days before rash and 7 days after onset Infants with congenital exposures can shed virus for more than a year Adults: 1-6 day viral prodrome, symptoms dissapear w/i 24 hours after rash develops Pink to red maculopapules; first on face then spreads rapidly DOWN to the trunk and extremities Lesions on the trunk tend to coalesce but those on extremities do not Rash remains for 1-5 days classically disappearing on the 3rd day Clearing may be accompanied by fine desquamation but usually not Lymphadenopathy begins days before the rash: suboccipital, postauricular, posterior cervical No specific treatment Complications Encephalitis Thrombocytopenia Arthritis Congential Defects 24% of infected fetuses have a congenital defect Maternal infection may be determined by serology: acute and convalescent increase in titers 4 fold is diagnostic Routine use of PEP in an unvaccinated women in early pregnancy is not recommended

ERYTEHMA INFECTIOUSUM = FIFTH DISEASE = SLAPPED-CHEEK RASH Parvovirus B19 infection Mild systemic symptoms, fever in 15%, characteristic rash Arthralgias and arthritis common in adults, rare in kids Slapped - cheek rash b/c of intensely red face with circumoral pallor Maculopapular lacelike rash in the arms, trunk, buttocks, and thighs Rash may recur with temperature changes

Incubation is 4 - 14 days Parvovirus: may also cause URTI, atypical rash, arthritis without rash Hepatitis can occur (rare) Aplastic crisis associated with parvoB19 and hemolytic anemias an sickle cell dz Pregnancy infection: fetal hydrops and death No treatment

SCARLET FEVER Clinical Features Recent decline in incidence Abrupt onset with fevers, chills, malaise, sore throat followed within 12-48hrs of distinctive rash: begins on chest and spreasds rapidly Circumoral pallor, sandpaper-like texture b/c of the rough feel of the skin due to the multitude of pinhead size lesion Pharyngitis +/- erythematous or petechial lesions on the palate After resolution of the symptoms, desquamation of the inovlved areas is characteristic Complications: abscess, OM, pneumonia, rheumatic fever, post strep GN Management Antistrep abx: penicillin V 50 mg/kg/day dividied qid in kids Pen V 250 po qid in adults Benathine IM injection X 1 is an option Erythromycin 250 mg (or 40 mg/kg) po qid if pen allergic X 10 days Need full 10 days b/c only literature to show prevention of rheumatic fever is with a 10 day course KAWASAKI DISEASE Acute vasculitis primarily of infants and children Previously named Mucocutaneous lymph node syndrome Peak incidence in spring and winter Majority occur < 5 yo; 1-2 yo is most common; RARE in adults Etiology unknown Immune system activation wth vascular injury as the result Myocarditis is the most common cause of death Fever, conjunctivits, rash, mucous membrane lesions, extremity changes, cervical lymphadenopathy Cervical adenopathy: 50%, may be presenting feature Fever: high, spiking, persistent for 1-3 weeks Conjunctivitis: bilateral, bulbar > palpebral, no exudate, mild uveitis Mucous membrane lesions: injected or fissured lips, injected pharynx, or strawberry tongue, no ulcerations Extremity changes: painful, erythematous, swollen hands and feet (may not be able to walk, may present with limp); desquamation of finger and toes begins 10-20 days after fever; Beau's lines are transverse grooves of the nail months after fever Rash: highly variable, appears within 5 days of fever, generally a maculopapular rash that may look like scarlet fever, urticaria, erythema multiforme, or morbiliform rash; may have small vesicles but no pustules or bullae

Arthritis common MCC of pediatric acquired heart dz: coronary artery aneurysms, coronary vasculitis, myocarditis, pericarditis, CHF, pericardial effusions, valve dz, arrtyhmias Coronary aneurysms: 20%; prone to MI or coronary rupture and tamponade; treatment with IVIG and high dose aspirin decreases incidence of coronary aneurysms to 3-5% Natural History Phase I: acute phase (1-2wks); fever, myocarditis, pericaridal effusions, other diagnostic signs Phase II: subacute phase (1-4 wks): fever/rahs/lymph nodes resolve and conjucntivitis persist; desquamation/arthritis/myocardial dysfunction occurs; highest risk of death Phase III: convalescent phase; clinical findings resolve, continues until ESR is normal 6-8 weeks after onset CDC Diagnostic Criteria = Unexplained fever for 5 days + 4/5 criteria C Conjunctivitis: bilateral w/o exudate R Rash E Extremity changes (red, swollen, desquamating) A Adenopathy (cervical ln, at least one > 1.5 cm) M Mucous membrane lesions (injected lips/pharynx, tongue)

Atypical Kawasaki's Cases that don't meet the CDC case definition More common in those < 6 months were diagnosis is more difficult Investigations Admit for echo Do ECG May need coronary angiogram CBC, lytes, creatinine, ESR, CXR, blood culture, urinalysis, ASOT titer, throat swab, LP if signs of aseptic meningitis Differential Diagnosis Rash: measles, toxic shock syndrome, Stevens-Johnson, RMSF, JRA, drug reaction, viral exanthem, scarlet fever H/N manifestations: RP abscess, GAS pharynitis, Mono Measles: severe cough, Koplik's spots Managment IV gamaglobulin: 2 g/kg over 12 hours (may need further treatments) High dose ASA: 100 mg/kg/day divided into q6hr dosing Therapy decreases incidence of coronary aneurysm

ROCKYMOUNTAIN SPOTTED FEVER Rickettsia rickettsii Transmitted to humans through tick bites (saliva at time of bite) Reported in North, South, and central america Most cases reported form SOUTHEASTERN USA Clinical Features Abrupt onset of headache, N/V, chills, fever to 40 degrees Ocassionally onset is more gradual with anorexia, malaise, fever May be prolonged (3 weeks)

May be severe (CNS, cardiac, pulomonary, GI, renal complications) Rash develops on 2nd - 4th day Erythemaous macules that blanch on pressure, appearing first on wrists and ankles then spreading up the extremities to the face and trunk w/i hours Lesions may become petechial or hemorrhagic Lesions on the palms and soles are particularly characteristic Increased capillary fragility and splenomegaly may be present Diagnosis Weil-Felix reaction (serology) Other immunologic flourescent procedures exist Treat based on suspicion b/c lab will be slow Management Tetracycline 25 mg/kg/day is the antibiotic of choice (po or iv) Doxycycline and chloramphenicol may be used as options Usual course is 10 days Avoid sulpha drugs which can exacerbate the illness Rickettsiae routinely resistant to penicillins, cephalosporins, aminoglycosides, and erythromycin PAPULAR AND NODULAR LESIONS CONTACT DERMATITIS Non - Allegic Contact Dermatitis Inflammatory reaction to chemical, physical, or biological agent Caustics, solvents, detergents cause irritant dermatitis Allergic contact dermatitis Delayed hypersensitivity reaction mediated by lymphocytes sensitize by the contact of the allergen to the skin Less common than (non-allergic) irritant contact dermatitis Clothing, jewelry, soaps, cosmetics, plants, medications contain allergens that commonly cause allergic contact dermatitis Rubber, poison ivy/oak/sumac (Rhus genus plants), paraphenyldenediamine (hair dyes and industrial chemicals), ethylenediamine (topical medication ingrediant) are the MCC of allergic contact dermatitis Sensitization to poison ivey results in sensitization to other similar plants: cashew, mango, lacquer, ginkgo trees Management Avoid irritant or allergen Treat secondary bacterial infections Wet compresses of Burow's solution for oozing or vesicular lesions (qid) Topical baths OTC Prednisone 50 mg po od if severe: taper over 14 days (21 for poison ivy) Taper of steroid needed to prevent relapse Antihistamines for pruritits Wash all clothes to remove offending agent that could be contaminated

DIAPER DERMATITIS Clinical Features Occlusive diapers and clothing, heat, moisture, friction, urine and feces all contribute Tends to SPARE CREASES Erythematous plaques in the genital, perianal, gluteal, and inguinal areas May extend elsewhere with more severe cases May be superinfected with candida: moist, red patches with well demarcated borders and papular or pustular satellite lesions May reflect atopic or seborrheic dermatitis in infants (especially if lesions are found elsewhere in the body) Management Remove excess clothing Remove occlusive diapers Frequent diaper changes Leave diapers off long enough to dry area Sterilized cloth diapers preferred Exudative lesions: wet compresses with saline or Burow's solution for 3/7 Zinc oxide (Desitin) may dry the area Hydrocortisone 1% cream in severe cases Avoid ointment based topical medications for treatment b/c their occlusive nature enhances moisture retention (use cream, not ointment) Nystatin cream or powder if Candida superinfection

ERYTHEMA MULTIFORME Etiology Drugs and HSV infections are the MCC Viral infections (heptitis, influenza) are next MCC Fungal infections: dermatophytosis, histoplasmosis, cocidiomyocosis Bacterial infections: strep and TB Collagen vascular disorders: RA, SLE, dermatomyositis, PAN Cancers Pregnancy DDX Urticaria Scalded skin syndrome Pemphigus Pemphigoid Viral exanthems Clinical Features Acute, self-limiting disease Erythematous or violaceous macules, papules, vesicles, or bullae Symmetrical distribution common Most common in PALMS and SOLES, back of hands or feet, extensor surfaces of the extremities Target Lesion with three zones of color is the hallmark: centra dark papule or vesicle, surrounded by a pale zone, a halo of erythema Steven - Johnson Syndrome = Toxic Exctodermal Necrolysis Severe form of EM

Bullae, mucous membrane lesions, MSOF Chills, malaise, headache, fever, tachycardia, hypotension Purulent conjunctivitis may occur and be severe Management Look for underlying etiology Resolve spontaneously in 2-3 weeks in mild forms Severe cases: admit, iv hydration, burn unit care, systemic analgesia, systemic corticosteroids Wet compresses with dressing soaked in 1:16000 solution of potassium permanganate or 0.05% silver nitrate several times a day to bullous lesions Look for infection and hypovolemia

PEDUNCULOSIS Clinical Features Nits or adult lice seen on microscopic examination of hair from symptomatic areas: nits are more common than the aduult louse form Nits attach tot eh bases of hair shafts looking like white dots Adult louse look like blue or black grains Severe itching and scratiching Secondary infections can occur Pediculosis corporis: lice live in clothing, bedding and feed on the host; the parasites are usually absent from the body except in very severe cases; Erythematous macules or wheals may be present with intense itching: Treatment consists of luandering or boiling the clothes and linen; may add lindane lotion if nits are found in the hair but this is usually not neccessary Pediculosis capitits: more common in small children; pruritis is the major sympom and may be confined to the scalp; excoriations and secondary bacterial Management Permetrhin (Nix) is the recommended treatment Lindand (Kwell) lotion or cream is no longer preferred Nix remains active for 2 weeks Avoid shampoos and conditioners for 2 weeks b/c it coats and protects the lice Nix: shampoo hair, dry, apply Nix, wash out after 10 minutes (MUST be applied when the hair is dry b/c lice don't breath for 30 min when immersed in water!); repeat dose one week after initial use Treat sexual partners Treat only symptomatic household members Wash clothes, sheets, pillow cases in hot water and dry in hot cycle Ivermectin 200 ug/kg and repeat in 10 days has been shown to eradicate lice SCABIES Clinical Features Mite infestation with severe itching Interdigital web spaces, flexion area of wrists, axillae, buttocks, lower back, penus, scrotum and breasts are the most common locations Infants have a more generalized involvement Reddish papules/vesicles surrounded by erythematous border and scratch marks Infants and young children often have generalized skin involvement includine scalp, palms, soles, face: most common presenting lesions are papules and vesiculopustules

Norwegian scabies: extensive hyperkeratosis and crusting of the hands, feet, and scalp; immunosuppressed patients; highly contagious Close personal contact transmission; multiple family members will usually have Management Permetrin 5% cream (Elimite) or crotamiton (Eurax) cream Lindane is no longer the preferred treatment Elimite: applied overnight once weekly for 2 weeks; cover the entire body (preferred treatment for infants and small children) Post scabietic nodules and pruritis may persist for months after sucessful tx Norwegian scabies requires repeated treatment Treat all family members and sexual contacts Wash and dry in hot temperatures the linens and underwear

SYPHILLUS Clinical Features Treponema pallidum Incubation 10 - 90 days Primary lesion: chancre, usually single lesion, lasts 3-12 weeks and heals spontaneously, appear at site of inoculation (genitalia or mucous membranes), chancre begins as a papules and characteristically develops into an ulcer approximately 1cm in diameter with a clean base and raised borders; painless chancre unless secondary infection; lymphadenopathy Secondary stage: 6weeks to 6 months with various different lesions Erythematous or pink macules or papulues, usually with a generalized symmettrical distribution Pigmented macules and papules classically appear on the palms and soles; may be scaly but rarely pruritic Papular, annular, circinate lesions are more common ion nonwhites Generalized lymphadenopathy and malaise accompany the lesions Irregular patchy alopecia Moist, flat, verucous condyloma latum may appear on genitals Diagnosis Primary: darkfield microscopy for spirochetes; not available in ED thus suspect and treat based on clinical suspicion and refer to STD clinic VDRL not very sensitive or specific in primary syphillus VDRL is better with secondary syphillus FTA-ABS serology is better (Florescent Treponema antibody absorption) Many causes of false +ve VDRLs: vaccines, mono, mycoplasma, etc Management Incubating syphillus (before chancre): 1gm of probenecid po then 4.8 million units of procain penicillin IM Primary and secondary: benzathine penicillin G 2.4 million units IM Doxycycline or tetracycline for pen allergic for 14 days Jarisch-Herxheimer reaction: febrile reaction and diffuse rash 12 hours after receiving treatment for syphillus, resolves spontaneously in 24hrs

ERYTHEMA NODOSUM Clinical Features Inflammation of the dermis and adipose tissue Painful red to violet nodules Nodules are elevated skin lesions located deep in the skin thus the overlying skin can be moved on palpation MC over anterior tibia but may be on arms or thrunk Fever and arthralgia of ankles may preceed the rash Lesions may turn yellow-purple and resemble bruises with evolution Most common in women in 20 - 50s Associations Infections: TB, sterptococci, yersinia, chlamydia, coccidio, histoplasmosis Sarcoidosis Ulcerative colitis and regional enteritis Pregnancy Idiopathich Drugs: OCP is the MCC Management Treat underlying condition CXR for ? sarcoidosis or TB should be considered Bed rest, elevate legs, wear stocking ASA 600 mg q4hr Resolves spontaneously in 4-6 weeks Potassium iodide 360 - 900 mg po od for 3-4 weeks if severe (? May act through an immunosuppressive mechanism mediated via heparin release from mast cells) VESICULAR AND BULLOUS LESIONS PEMPHIGUS VULGARIS Clinical Features Vesicles = elevated lesions that contain clear fluid Bullae = vesicles > 1 cm Pemphigus vulgaris is an uncommon but severe disorder Bullous disease most common in 40 - 60yo Small, flaccid bullae that break easily forming superficial erosions and crusted ulcerations are the typical lesions Any area of the body may be involved Nikolsky's sign is present 60% have mucous membrane lesions Oral lesions typically preceed the cutaneous lesions by months Gums and vermilion borders of lips are particularly common Oral lesions are bullous but break easily thus superficial ulceration is seen Cause unkonwn Has been seen rarely with captopril and penicillamine Tzanck cytologic test suggest the diagnosis (finding acanthyolytic cells, degenerated rounded epithelial cells with amorphous nuclei) Acantholytic cells are not specific for pemphigus Serum immunofluorescence confirms the diagnosis

Ddx: bullous pemphigoid, epidermolysis, dermatitis herpetiformis, TEN, bullous scabes, bullous SLE Management Pain control Local wound care Steroid: 100 - 300 mg prednisone Consult dermatology Other immunosuppressants sometimes used Mortality very high without steroids Superinfection and complications of steroids are problematic

PEMPHIGOID HERPES SIMPLEX HSV 1: primarily nongenital areas HSV 2: primarily genital areas Clinical Features HSV 1 most common in mouth, more common in children Cluster ov vesicles that appear, break and leave crusted erosions Can have very severe gingostomatitis with dehydration Secondary infection with staph and strep can occur Hallmark = painful group of vesicles on erythematous base Usually nondermatomal distribution Avoid contact with atopic dermatitis kids b/c of severe generalized HSV can develop in kids with atopci eczema and other dermatosis HSV2: single or grouped vesicles on penis, prodrome of local pain and hypesthesia common, constitutional symptoms and L.N. common Versicles erode over few days, become crusted, and heal over 2 weeks Located to cervix, vagina, or introitus in women Herpes cervicitis may cause severe pelvic pain in women Managment First episode of gential herpes: acyclovir (Zovirax) 200mg po 5X/day X 10/7 Famciclovir or vancyclori are options Treat until resolution of lesions if not gone by 10 days Improve healing and decrease spread with treatment but do NOT prevent recurrences (acyclovir prophylaxis may help suppress herpes) Acyclovir can be started at first sign of recurrence Immunocompromised: admit for iv acyclovir Pain control important Treat partner Stomatitis: Maalox and benadryl (?treat primary gingivostomatitis with acyclovir)

VARICELLA Clinical Features Chickenpox; Varicella-zoster virus Incuation 2-3 weeks Begins with low fever and constitutional sympomts Exanthe4m conincides with these sympomts in children but follows them in adults by 1-2 days Lesions rapidly progress from macules to papulues to vesicles to crusting lesion sometimes within hours; vesicles are 2-3 mm and surrounded by erythematous border (can have larger bullae) Drying vesicles produce scabs which fall off in 5-20 days Highest concentration in trunk Hallmark = lesions in all stages (macules, papules, vesicles, crusts) Complications Bacterial superinfection of lesions Secondary bacterial pneumonia Encephalitis Thrombocytopenia Arthritis Hepatitis Glomerulonephritis Management Symptomatic treatment AVOID ASA (Reye's syndrome) Oral acyclovir may be effective if started within 24hours of rash for patients with chronic respiratory or skin diseases; may decrease duration and symptoms Isolation usually futile b/c spread before diagnosis: keep at home though becouse spread continues until all vesicles have crusted over and dried up Varicella vaccination exists Maternal varicella 5 days before and 2 days after delivery can result in disseminated herpes in the newborn Pregnant women and immunocompromised exposed to chicken pox Check varicella-zoster titers VZIG must be given to those with negative titers who are exposed Congenital anomalies if exposed in first or early second trimester: embryopathy, limb atrophy, scarring extremities, CNS and ocular manifestations HERPES ZOSTER Clinical Features Shingles is an infection caused by varicella zoster virus Virus lives in dorsal root ganglion and is reactivated Pain in dermatome prior to appearance of rash by 1-10 days Grouped vesicles on erythematous base in dermatomal pattern Thorax and trigeminal nerves are the MC location Vesicles appear then b/cm cloudy and progress to crusts and scabs Crusts fall off at 2-3 weeks Peak incidence in 50 - 70yo (rare in children) Associations: leukemia, Hodgkin's, other cancers (don't need to hunt for) You CAN acquire chicken pox from exposure to shingle but uncommon

Can be a disseminated infection Complications: ocular infection, postherpetic neuralgia, meningoencephalitis, myelitis, peripheral neuropathy Ocular: 20 - 70% involve the opthalmic division of trigeminal nerve (V1); can be vision threatening; anterior uveitis, conjunctivitis, secondary glaucoma, corneal scarring can all occur; tip of the nose means that the nasociliary nerve is involved and predicts eye involvement More severe in immunosuppressed especially AIDS, Hodgkin's, other lymphoma; cutaneous and CNS dissemination more common in these groups Postherpetic neuralgia More common in elderly and immunocompromised May lasts months to years Management Analgesia Other treatment rarely necessary Burow's solution may be applied to hasten drying Steroids: may shorten duration of postherpetic neuralgia but does not lesson the severity of pain or affect the rate of healing Acyclovir, famciclovir, valacyclovir etc: have been shown to be effective for immunocompromised patients Capsaicin cream can be used on areas with postherpetic neurlagia\ Severe ocular zoster: iv acyclovir may be of some benefit, topical steroids (is used with zoster; is NOT used with herpes simplex conjunctivitis)

PUSTULAR LESIONS IMPETIGO Principles Slowly resolving pustular eruption most common in preschool children Staph aureus is the most common cause currently Group A strep is the second MCC Predispositions: eczema, poor hygeine, malnurished, other skin conditions Clinical Features Streptococcal impetigo (ECTHYMA) Most common on the face Begins as a single pustule but then develops into multiple lesions: 1-2mm vesicles with erythematous margins; when they break they leave red erosions covered with a golden yellow crust Can be pruritic but are not paiful Regional lymphadenopathy common Very contagious among infants and children (less in older) Post strep glomerulonephritis as a complication Staphlococcal impetigo Little surrounding erythema compared to strep Staph is a more superficial infection Bullous impetigo Caused by staph phage group 2 Primarily in infants and young children

Initial lesions are thin walled 1-2cm bullae; they rupture to leave a thin serous crust and collarette-like remnant of the blister roof at the rim of the crust Face, neck, extremities are most common Ddx: dermatitis, HSV infection, fungus, pemphigus vulgaris Gram stain of fluid from bullae: Gram+ve cocii Management Systemic and topical antibiotics are equally effective More extensive lesions should be treated systemically NO evidence that antibiotics prevent post strep GN Mupirocin 2% ointment tid Erythromycin qid X 10/7 or Keflex are options Bullous impetigo: penicillinase resistant semisynthetic penicillin (dicloxicillin) or erythromycin; add mupirocin 2% ointment to area as well FOLLICULITIS Inflammation of the hair follicle Usually caused by staph aureus Lesions are on usually on buttocks, thighs, and occasionally scalp/beard Ddx: acne, keratosis pilaris, fungal infection Pseudomonas associated with hot tubs, pools, antibiotic use for acne Gram stain of lesion can tell pseudomonas from staph Mx: antiseptic cleaner (chlorhexidine) daily until cleared Extensive involvement: erythromycin, dicloxacillin may be added

CARBUNCLE Large abscess that develops in thick inelastic skin of back of neck, back, thighs Severe pain, fever, sepsis possible Local heat I&D when fluctuance present Abx only necessary if cocomitant cellulitis or sepsi

HIRADENITIS SUPPURATIVA Apocrine sweat glands Recurrent abscess formation in axilla and groin resembles furunculosis Recurrence common; often resistant to therapy Need to I&D abscesses Antistaph abx useful if early and long course used Many require local incision and skin grafting Antiandrogen therapy is an option in resistant cases GONOCOCCAL DERMATITIS Arthritis - dermatitis syndrome MC presentation of disseminated gonococcal disease 2% of patients with gonnococcus (MC in women) Fever, migratory polyarthralgias, skin lesions Multiple lesions with predominance for periarticular regions of distal extremities

Erythematous or hemorrahgic papules that evolve into pustules and vesicles with an erythematous halo (look like meningococcemia). They are tender and may have a gray necrotic hemorrhagic center. Healing with crust formation usually occurs w/i 4-5 days Recurrent crops of lesions can occur even after antibiotics started Gultures and gram stains of lesions usually negative Immunofluorescent antibody staining of direct smears from pustules more reliable Diseminated gonococcal infection Ceftriaxone 1gm iv/im q24hrs OR cefotaxime 1gm q8hr Allergic to Blactams: spectinomycin 2 gm im q12hrs Switch to po cefixime, cefuroxime, cipro, or ofloxacin Total treatment of 7 days Hospitalization for septic arthritis, meningitis, endocarditis

PETECHIAL AND PURPURIC LESIONS INTRODUCTION Purpura = blood in the skin or mucous membrane; divided into petechiae and echymosis Petechia = small, <0.3mm reddish-purple macular lesions Ecchymosis = larger lesions that are often tender and may be raised PURPURIC LESIONS DO NOT BLANCH Vascular dilation or vascular anomalies will blanch (spider angiomas for example) Characteristic resolution: purple ­> golden-brown -> yellow DIFFERENTIAL DIAGNOSIS OF PURPURIC RASH VASCULAR INTEGRITY PROBLEM Trauma: normal and Non-Accidental trauma must be thought of Infections: meningococcus, viral NOS, mono, endocarditis, ricketssia, strep Drugs HSP and other vasculitidies (kawasaki's, serum sickness, cryoglobulinemia, vasculitis with SLE/lyme/IVDA/PBC) Vit C deficient Ehlers-danlos etc PLATELET PROBLEM Thrombocytopenia Decreased production Sepsis: esp meningococcus Drug suppression Aplastic anemia BM infiltration Increased destruction Sepsis/DIC Drug HUS TTP ITP Increased sequestration Liver dz

Splenomegaly Platelet Dysfunction Chronic renal failure, aspirin and other drugs Congenital platelet disorders COAGULATION FACTOR PROBLEM Congenital Hemophilia A/B Von-Willebrand factor Christmas tree factor def Acquired DIC Warfarin Vit K deficiency Liver dz, renal dz

APPROACH TO THE PURPURIC RASH MUST consider non-accidental trauma Other causes of sepsis actually more common than meningococcus for the sick purpuric rash The well looking person/child with a petechial rash? Is it meningococcemia???? Many infections can cause petechiae or ecchymosis in absence of platelet or coagulation disorder Capillary damage from the infection Rubeola, mono, ricketsia, streptococcal, RMSF, endocarditis can all present Keep in mind the above ddx: vascular integrity problem, thrombocytopenia, coagulation factor problem Approach Toxic appearing: monitored bed, iv access, draw labs, fluid bolus, draw cultures, start antibiotics, resuscitate as needed History and Physical: drugs, infectious symptoms, bleeding history, easy bleeding or brusing, lumps or bumps, weight loss or systemic symptoms, full review of symptoms Order: CBC, diff, platelet count, retic count, PTT, INR, bleeding time Thrombocytopenia Prolonged INR/PTT: sepsis and DIC Normal INR/PTT: ITP, TTP, HUS, bone marrow suppression, bone marrow infiltration, platelet sequestration Platetlets normal, INR/PTT prolonged Hemophilia Liver dz Warfarin Platelets normal, INR/PTT normal, Bleeding Time prolonged Von-Willebrand disease Aspirin or other platelet inhibitors Platelets normal, INR/PTT normal, Bleeding Time normal Vasculitis: HSP, serum sickness, cryoglobuinemia, IVDA, kawasaki's Trauma Infections

Drugs Connective tissue disease

MALIGNANCY AND DERMATOLOGY ACANTHOSIS NIGRANS Most do NOT have tumors but some do Malignant acanthosis nigrans: = associated with cancer (skin lesion itself is NOT cancer) Hyperpigmented verrucous velvet - like hyperplasia and hypertrophy of the skin with accentuated skin markings: body folds, especially axillae, antecubital fossae, neck and groins MC is adenocarcinoma of the stomach Others: breast, ovary, pancreas, colon, uterus Tumor produces insulin-like growth factor which stimulates the skin DERMTOMYOSITIS Some will have underlying malignancy Breast, ovary, GI, uterus ERYTHEMA MULTIFORME Associated with leukemia Also Hodkin's ERYTHRODERMA Almost pathognomonic of Hodgkin's lymphoma Also occurs with lymphocytic leukemia ACQUIRED ICHTHYOSIS Generalized dryness of skin, scalin, superficial cracking, or hyperkeratosis of soles and palms Hodgkin's is MCC Other cancers also PRURITIS Hodgkin's lympoma, leukemia, adenoCa, Sqcell Ca, carcinoid, multiple myeloma Hodgkin's may have severe itching and burning sensations Standard treatments ineffective PURPURA MC manifestation of acute granulocytic and monocytic leukemia Also myeloma, lymphoma, polycthemia vera Thrombocytopenia secondary to BM suppression is the mechanism Non-thrombocytopenic forms do occur URTICARIA Hodgkins Leukemia Internal carcinomas

NARCOTIC ADDICTION Skin needle tracks: indurated linear hyperpigmented streaks Skin popping: subcutaneous injections result in round or oval hyperpigmented atrophic depressed scars 1-3 cm in diameter Skin abscesses Hypertrophic keloid scars Increased pigmentation at site of tourniquet use


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