Triamcinolone 0.1% cream; comes in 1 pound jar
can give IM as well
10mg = 1 week
40 mg = 4 weeks
needs to be deep muscle injection upper outer buttocks
for weeping dermatitis
steroids for sensitive areas
Common Skin Lesions
· Macule-circumscribed area of change in skin color
· Papule-solid raised lesion up to 5mm
· Nodule-like a papule but deeper in dermis or subcutaneous tissue, > 5mm
· Plaque-circumscribed elevation of skin >5mm, large papule
· Pustule-raised area of skin containing pus
· Vesicle-elevated fluid filled lesion up to 5 mm
· Bulla-elevated, fluid filled lesion >5mm
· Petechiae-red or brown macules up to 5mm that do not blanch
· Purpura-ptechiae >5mm
· Scales-dead epidermal cells
· Erosion-loss of only epidermis, no scar c healing
· Ulcer-loss of epidermis and dermis
· Excoriation-linear or angular erosions from scratching
· Crust-collection of dry serum and cellular debris
· Lichenification-area of thickened epidermis from chronic rubbing
· Atrophy-depression in skin from thinning epidermis
Red Flags of Life Threatening Rash
· Fever: consider viral exanthem, septicemia, RMSF, TSS, erythema multiforme, Kawasaki, Stevens-Johnson, TEN
· Very Young: meningococcemia, Kawasaki, viral
· Elderly: meningitis, pemphigus vulgaris, sepsis, meningococcemia, TEN, Stevens-Johnson, hypersensitivity syndrome, TSS
· Toxic: necrotizing fasciitis, meningococcemia, TEN, Stevens-Johnson, hypersensitivity, TSS, RMSF
· Immunocompromised: Meningococcemia, herpes zoster, septicemia, necrotizing fasciitis (ETOH, Asplenia, Debilitated)
· Adenopathy: drug reaction, hypersensitivity, viral
· Diffuse Erythroderma: staph scalded skin, TSS, Strep TSS, nec. Fasciitis
· Ptechiae/Purpura: meningococcemia, nec. Fasciitis, DIC, RMSF
· Mucosal/Oral Lesions: Erythema Multiforme, TEN, Stevens-Johnson, Kawasaki, pemphigus
· Hypotension: TSS, meningococcemia, RMSF, TEN, Stevens-Johnson
· Recent New Drug Use: drug rxn, photosensitivity, EM, TEN, S-J, hypersensitivity
· Arthralgias: RMSF, drug rxn, viral
· When did the rash start? How quickly did it progress? The more lethal, the more rapid the progression.
· Did the rash change over time? Anthrax begins as a pruritic papule progressing to an ulcer and then eschar a week later?
· Where did the rash start and how did it progress? Vasculitic rashes spread peripheral to central, viral rashes spread central to peripheral.
· Is the lesion pruritic? Itching is a primitive form of pain mediated by histamine release. Usually signifies some form of allergic response
· Recent Travel? RMSF, Lyme, Typhus (SW US), Hemorrhagic Fevers (Africa)
· PMH? Ask about immunocompromise, asplenia, etoh use, cancer, diabetes
· Occupation? Daycare workers, military, and students predisposed to meningococcemia. Tularemia in gametrappers.
Get pt naked. Check oral cavity, adenopathy, hepatosplenomegaly, genitalia, nails and fingers
1. Characterize the Type of Lesion
2. Shape of individual Lesions
3. Arrangement of multiple lesions (linear, annular, serpiginous, or disseminated)
4. Pattern of Rash (ie. Sun exposed areas, flexor/extensor surface, symmetrical, etc.)
Most common rash presentation with a broad differential
Viral Exanthems (centrally distributed)
Measles-Koplik’s spots, blueberry muffin spots, rash progresses face to feet
Roseola Infantum-Sixth Disease
Rubella-face to feet, maculopapules
Erythema Infectiosum-5th disease, slapped cheek
Scarlet Fever-post strep, sandpaper
Cutaneous Drug Reactions
Most commonly caused by sulfonamides, penicillins, anticonvulsants, and NSAIDS
Either morbilliform (looks like measles) or exanthematous.
Erythematous macules and papules mainly on trunk and extremities
Pts c mononucleosis who take ampicillin get non-immune rash of this type
Hypersensitivity syndrome is a severe form usually 2-6 weeks after taking drug with exanthematous rash that may exfoliate combined with fever, hepatitis (get LFTs), nephritis, carditis, and lymphadenopathy.
Treatment: stop any drugs that can be safely held. Give antihistamines for itching.
drug rash with eosinophilia and systemic symptoms
high and long lasting fever macular erythematous rash which usually begins on the trunk and the abdomen
itchy and may feature papules or pustules
lymphadenopathy, hepatitis, 1/3 patients have eosinophilia
withdraw the offending agent
Unknown etiology, cause not found in half of cases. May be post-viral. ? from drug reactions
Chief complaint is of rash with prodrome of malaise, fever, and arthralgias.
Present with target lesions
Dusky red macules and papules appear on palms, soles, and extensor surfaces of extremities, especially the knees and elbows. Usually symmetrical, evolving over 24-48 hours. As the lesions enlarge, central area becomes cyanotic with dusky centers. Non-pruritic, usually 1-2 cm in size.
Lesions usually heal in 1-2 weeks, entire episode can last a month.
EM minor is just the skin lesions without bullae or severe systemic symptoms; these pts may be discharged
If one mucous membrane (lips, oral cavity, or conjunctiva) is involved then disease becomes EM Major. Separation between EM and S-J/TEN is nikolskys sign. Up to 10% have ocular involvement which can lead to permanent blindness.
Treatment: ? of prednisone, data is scant. Antihistamines if pruritis. Optho consult if ocular involvement
EN is considered an immunologic response, and the three most common etiologies in North America are: streptococcal pharyngitis: EN typically appears 2 to 3 weeks after the onset of pharyngitis sarcoidosis: often presents with EN and bilateral hilar adenopathy. medications: most commonly oral contraceptives, but also antibiotics, notably the sulfonamides. In the southwestern US, however, coccidiomycosis is the most frequent cause
Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis
From drug reactions (most implicated Sulfonamides, NSAIDS, anticonvulsants, Abx)
Chief complaint is a rash, possible flu-like prodrome. Prodrome may begins days after drug ingestion, skin lesions 1-2 weeks later. Lesions are target lesions on the trunk (in contrast to EM where the majority of the rash is on the extremities and face>) Oropharyngeal lesions can progress to stomatitis. Purulent conjunctivitis which can lead to blindness and ocular erosions. The skin lesions usually resolve in a month. TEN also has pruritis, pain, and tenderness in association with the skin lesions.
Nikolskys sign: lateral pressure of normal skin adjacent to lesions dislodges epidermis.
Bullae form between the dermis and epidermis leading to widespread sloughing of skin.
In TEN, mucous membrane involvement is common, including genital and anal lesions.
SJS has <10% of epidermal detachment
TEN >30% epidermal detachment
In between is an transition zone between the two.
Biopsy can confirm the skin lesions and differentiate from Staph Scalded Skin.
Treatment: supportive care and aggressive fluid management. Discontinue all drugs started in the past month. Large risk of infection from breakdown of skin barrier
Rare blistering condition seen in 40-60 y/o age group. From circulating IgG.
Initially with blisters on oral mucosa for weeks to months before the skin is involved. Non-pruritic skin blisters then erupt over several weeks. Usually effects the head and trunk first and then generalizes.
With slight pressure, blisters will rupture (Nikolsky’s). Ruptured blisters form secondary erosions which are very prone to infection.
Official diagnosis is by biopsy adjacent to a blister.
Treatment: 1 -2 mg/kg/day of prednisone until remission. If only a few blisters can go home, but if pt appears toxic, admit.
· Pneumococcal Sepsis
· H. Flu Sepsis
· Rat Bite Fevers
· Epidemic Typhus
· Hemorrhagic Fevers
· Enteroviral Infections
· Hep B
· Valsalva (petechiae above the nipple line)
· Vasculitis (HSP, Hypersensitivity)
Consider isolation. Consider all pts to have meningococcemia or RMSF until proven otherwise.
Inquire about sick contacts, travel history, tick bites, medical history.
Palpable purpura from HSP, cyroglobulinemia, hypersensitivity, vasculitis
No febrile child with ptechiae solely above nipple line had invasive disease (Pediatrics 84 (6) 1989)
CBC, Blood CXs, Chemistries, PT/PTT, UA (for HSP) . LP if meningeal.
General Treatment: if pt is apparently infectious, give Ceftriaxone 2 g and Doxy 100 mg IV to cover all life threats.
Colonization of nasopharynx leading to CNS invasion or septicemia. Asplenic pts or those with complement deficiency are most at risk. Usually begins 3-4 days after exposure. Flu-like prodrome. Rash is present in 70% of pts. Petechiae on the wrist or ankles is usually the first sign. Can lead to fulminating septicemia (waterhouse-friderichsen syndrome) c hemorrhagic destruction of the adrenal glands.
Primarily affects peds
Cutaneous palpable purpura on legs and buttocks, arthritis, abd pain, gi bleeding and nephritis. IgA is the mediator.
Steroids are helpful, but the disease is usually self limiting.
Diffuse Erythematous Rashes
Staph Scalded Skin
Tinea Capitis- topical or griseofulvin
Candida-if oral nystatin swish and swallow
Gonococcal Dermatitis presents c arthritis
Cutaneous Larva Migrans:
CLM is a serpiginous skin eruption caused by burrowing larvae of animal hookworms. Usually the offending agent is the dog or cat hookworm, Ancylostoma braziliense. The larvae hatch from eggs passed in the dog and cat feces and mature in the soil. Humans become infected after skin contact with soil in areas frequented by dogs and cats. After the larvae penetrate the skin, erythematous lesions form along the tortuous tracts of their migration as they search for the intestines. Never making it that far, the hookworm larvae do not mature in humans and, without treatment, will die out after several weeks, with resolution of skin lesions. The lesions are intensely pruritic and may occur anywhere on the body. They can be numerous if the patient has lain on the ground. The lesions are well demarcated, like ringworm, and can have a ring-like geometry, again similar to ringworm. The treatment of choice is topical thiabendazole applied 2 to 3 times per day for 5 days. If topical treatment fails, oral albendazole (200 mg bid for 2 days) or oral ivermectin (150 to 200 µg/kg one time) are preferred due to the high frequency of adverse effects with oral thiabendazole.
Individual nodulocystic and large pustular lesions can be effectively treated with a single injection of triamcinolone acetonide delivered with a 27- or 30-gauge needle. Commercial preparations include Kenalog (10 mg/ml) and Tac-3 (3 mg/ml). The 10 mg/ml suspension can be used at full strength or diluted with 1% Xylocaine or physiologic saline. Saline is preferred because injections of Xylocaine mixtures are painful. A 2.5 to 5.0 mg/ml concentration is usually an adequate injection for suppressing inflammation.
The bottle of steroid solution needs to be shaken thoroughly in order to disperse the white suspension. The syringe should be shaken immediately prior to injection. The needle is inserted through the thinnest portion of the cyst roof and 0.1 to 0.3 ml of solution is deposited into the cyst cavity. This quantity momentarily blanches most cysts. Atrophy may occur if steroids are injected into the base of the cyst. Patients should be assured that if skin depression does occur, in most cases it is temporary and gradually resolves in 4 to 6 months. Multiple cysts can be injected in the course of one session. Intralesional injection is used specifically to supplement other programs.
Toxicodendrons (Poison Ivy and Oak)
Four types of reactions: contact urticaria; irritant dermatitis; phytophotodermatitis (often seen with limes, parsley, and celery); allergic contact dermatitis
Contact urticaria: contact with irritant that immediately causes hives; some substances cause photosensitization to sun; nettle leaf hairs classic example (cause wheals in 3 to 5 min that stay red for 1.5 hr; tingling can last 12 hr or longer); toxin-mediated reaction (anybody who touches plant will have reaction), not immunologic reaction (only those who are sensitized will react)
Irritant dermatitis: can be mechanical (due to spines or thorns) or chemical (toxin-mediated; leaves pattern); thorns can cause foreign body granulomas and, if in bones or joints, can cause tenosynovitis, chronic arthritis, and periosteal reaction; thorns can cause secondary infection with Clostridium tetani, Staphylococcus aureus, Sporothrix schenkii (thorns from roses packed in sphagnum moss; infection spreads via lymphatic system), atypical mycobacteria (not easily cultured)
Phytophotodermatitis: phototoxic reaction; phototoxicity can be immediate or delayed; caused by combination of topical photosensitizing agent followed by UV light; UVA sensitivity peaks in 0.5 hr to 2.0 hr; occurs only on sun-exposed skin; bergapten (5-methoxypsoralen) photosensitizing agent in limes (more plentiful in rind than pulp)
Allergic contact dermatitis: caused by poison oak, poison ivy, and poison sumac; all have three leaves and contain urishiol; urishiol also contained in mango (rind and stem), Florida holly, cashew tree, and gingko tree; mild soap and gentle washing removes urishiol (rubbing alcohol may help dissolve oils); bleach not helpful and can ruin skin; 50% of resin can be removed 10 min after exposure, 25% after 15 min, 10% after 30 min, none after 60 min; delayed cell-mediated hypersensitivity reaction; generally takes 48 to 72 hr; if patient exposed as child and again as adult, may take up to 5 days for reaction to occur; if patient exposed that summer, reaction may occur in 24 hr; when patients present with rash, ask them what they were doing 2 to 5 days ago; rash lasts 2 to 3 wk; dose pack of Medrol (methylprednisolone) lasts 1 wk, resulting in patients feeling better, rash returning, followed by patients thinking they were exposed again (give them enough); crushed plants leak offending oil; if following group through poison ivy, go through leaves that have not been broken; unbound oil on clothes, shoes, tools, pets, etc, stays active for months and can cause recurrences
Rash: develops like photography film, ie, area of greatest exposure breaks out first (exposure to leaf followed by exposure to stem); pattern that develops looks like rash spread by scratching, but cannot spread by scratching once oil bound to skin; blister fluid contains serum only; can wipe oil onto another person, but if youre rashy, the rash isnt going to spread it to somebody else; persistent rashes usually caused from repeat exposure
Prevention: learn to recognize poisonous plants; use lotion-based skin barriers prior to exposure (eg, Ivy Shield, IvyBlock, Work Shield, Tecnu); 70% of population thought to be capable of becoming sensitized to poison ivy; some become allergic after one exposure, others take years; wash skin promptly after exposure (alcohol or mild soap and water); launder clothing promptly
Treatment: systemic steroids probably should be used in patients with severe cases; cold compresses and antihistamines helpful; Lidex (fluocinonide) gel soothing and cooling and helps evaporation on wet eczematous rash; clobetasol too strong; prednisone tablets for severe cases (60 mg every morning for 5 days, followed by 30 mg every morning for five days, followed by 20 mg every morning for 5 days); by time patients present, they probably have had rash for 1 wk, so only need to cover for 2 wk; injection of Kenalog (triamcinolone; 60 mg) will start drying rash within 1 day; prednisone gives some patients difficult side effects
Consider Use of Maalox (Acad Emerg Med 10:688, 2003)
Pityriasis rosea Adam O Goldstein, MD, MPH Beth G Goldstein, MD UpToDate performs a continuous review of over 330 journals and other resources. Updates are added as important new information is published. The literature review for version 13.3 is current through August 2005; this topic was last changed on November 2, 2004. The next version of UpToDate ( 14.1) will be released in February 2006. INTRODUCTION Pityriasis rosea is an acute, self-limited, exanthematous skin disease characterized by the appearance of slightly inflammatory, oval, papulosquamous lesions on the trunk and proximal areas of the extremities. The diagnosis and management of this disorder are reviewed here. ETIOLOGY A viral etiology for pityriasis rosea (PR) has been hypothesized based upon the following observations: PR is sometimes preceded by a prodrome. It occasionally occurs in small case clusters. It has not been shown to be associated with bacterial or fungal organisms. This supposition is reinforced by the finding of viral-like particles in PR biopsy specimens examined with the electron microscope [ 1]. A significant literature supports the hypothesis that PR is a manifestation of human herpesvirus 7 (HHV-7) reactivation [ 2]. However, others have failed to detect HHV-7 DNA sequences and antigens in a significant number of PR cases, arguing against a causative role for this agent . More study is needed before this issue can be definitively resolved. CLINICAL FEATURES Pityriasis rosea (PR) is largely a disease of older children and young adults. It is slightly more common in women than men. A prodrome of headache, malaise, and pharyngitis may occur in a small number of cases, but except for itching, the condition is usually asymptomatic. The eruption commonly begins with a “herald” or “mother” patch, a single round or oval, rather sharply delimited pink or salmon-colored lesion on the chest, neck, or back, 2 to 5 cm in diameter. The lesion soon becomes scaly and begins to clear centrally, leaving the free edge of the cigarette paper-like scale directed inwards toward the center. A few days or a week or two later oval lesions similar in appearance to the herald patch, but smaller, appear in crops on the trunk and proximal areas of the extremities ( show picture 1 and show picture 2 and show picture 3 ). The long axes of these oval lesions tend to be oriented along the lines of cleavage of the skin. This characteristic arrangement is most evident on the back where it is emphasized by the oblique direction of the cleavage lines in that location ( show picture 1). The eruption spreads centrifugally or from the top down for a few days. Erythema gradually subsides, desquamation is completed, and the eruption fades, leaving little residual changes, except occasional mild post-inflammatory changes in light skinned individuals. Most cases are clear in four to six weeks; occasionally the disease will persist for several months. PR generally has only mild effects on quality of life, at least in children . The erythema may be difficult to see in darker-colored skins, and post-inflammatory pigmentation may be prominent, persisting for several months or longer. In children the distribution of the lesions is often atypical, involving the scalp and face; it may be completely “inverse,” affecting the face and distal extremities, while sparing the trunk. The lesions themselves also are sometimes atypical in children; they may be folliculo-papular, vesicular, pustular, urticarial, or purpuric. DIAGNOSIS The presence of a herald patch by history or on examination, the characteristic morphology and distribution of the lesions, and the absence of symptoms other than pruritus combine to make PR an easy diagnosis in most instances. However, the herald patch can resemble tinea corporis so closely that KOH examination of scales for dermatophyte hyphae may be necessary to distinguish these conditions. There are typically no laboratory abnormalities with PR. Skin biopsy is rarely necessary, but when performed shows focal parakeratosis with or without acanthosis, spongiosis, a perivascular infiltrate of lymphocytes and histiocytes, and occasionally extravasation of red cells. The biopsy picture is characteristic, but not pathognomonic. In doubtful cases signs, symptoms, and laboratory abnormalities relevant to the conditions listed in the differential diagnosis list will assist in proper identification. Differential diagnosis Psoriasis, secondary syphilis, tinea corporis, Lyme disease, HIV seroconversion illness, and drug eruptions must be considered in the differential diagnosis of PR. Therapeutic gold injections also can cause eruptions that mimic PR closely; these eruptions do not represent allergic reactions, but are dose-related and can be managed safely by reduction in dose size and the frequency of administration . Other medications and procedures more recently suspected of producing PR-like reactions are omeprazole [ 6], terbinafine [ 7], bone marrow transplantation [ 8], interferon alpha 2A [ 9], naproxen  , captopril [ 11], isotretinoin [ 12], and bacillus Calmette-Guerin therapy [ 13]. TREATMENT Most cases of PR need no treatment other than reassurance and proper patient education ( see “Patient/parent education” below). Topical steroids in the middle potency range are helpful in the control of itching ( show table 1A-1B). They can be applied to the pruritic areas two or three times daily. Topical antipruritic lotions such as prax, pramagel, or sarna may also be helpful. Referral to a dermatologist for phototherapy may be considered in patients who have severe itching, extensive disease, and who cannot expose themselves to noon time natural sunlight. UVB phototherapy decreases disease severity during periods of treatment, although it has less effect upon itching and overall disease outcome than previously thought . A trial of erythromycin may be useful in unusually severe cases of PR. One well-controlled study of 90 patients found that erythromycin by mouth (250 mg four times daily for 14 days) was effective in reducing both the duration and the severity of the disease . In this report, a complete response at six weeks of follow-up was noted in 73 percent of patients in the treatment group compared with none in the placebo group. A positive effect of erythromycin may stem more from antiinflammatory and immune modulating effects rather than antimicrobial effects . Follow-up Patients should be advised that the rash may persist for two to three months; no follow-up is necessary as long as it resolves within this time. New lesions may occur during this period but should disappear spontaneously. Patient/parent education Parents of children with PR typically want information about etiology (not really known), infectivity (thought to be very low), relapse (unusual), and complications or dangers (rare) .
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