Rash Without Fever

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Transcript of Rash Without Fever

Rash without feverNithin .v.Krishnan

History of Present Illness: Time of rash onset, location, pattern of spread (chest to extremities). Associated sympyoms Fever, malaise, headache; conjunctivitis, coryza, Treatments tried Exposure to persons with rash, prior history of chicken pox. Sore throat, joint pain, abdominal pain. Exposure to allergens or irritants. Sun exposure, cold, psychologic stress.

Past Medical History: Prior rashes, asthma, allergic rhinitis, urticaria, eczema, diabetes, hospitalizations, surgery. Medications: Prescription and nonprescription, drug reactions. Family History: Similar problems among family members. Immunizations: Vaccination status, measles, mumps, rubella. Social History: Drugs, alcohol, home situation. Birth history for neonates Was the mother ill? Did the mother have any medications?

Physical Examination General Appearance: Respiratory distress, toxic appearance. Vital Signs: Temperature, pulse, blood pressure, respirations. Skin: Complete skin examination, including the nails and mucous membranes. Color or surface changes, texture changes, warmth. Distribution of skin lesions (face, trunk, extremities), shape of the lesions, arrangement of several lesions (annular, serpiginous , dermatomal); color of the lesions, dominant hue and the color pattern, surface characteristics (scaly, verrucous), erythema, papules, induration, flat, macules, vesicles, ulceration, margin character, lichenification, excoriations, crusting. .

Eyes: Conjunctival erythema. Ears: Tympanic membranes Mouth: Soft palate macules; buccal mucosa lesions. Throat: Pharyngeal erythema. Lymph Nodes: Cervical, axillary, inguinal lymphadenopathy. Chest: Rhonchi, crackles , wheezing. Heart: Murmurs Abdomen: Tenderness,masses,hepatosplenomegaly. Extremities: Rash on hands, feet, palms, soles; joint swelling, joint tenderness.

Vesiculobullous lesions Age of onset Neonatal-genetic, infectious, or even iatrogenic. If the lesions are congenital, a genetic blistering disorder should be considered. Some autoimmune disorders can be transferred through the presence of maternal antibodies, up to about 6 months of age. include neonatal lupus, neonatal pemphigus, and pemphigus foliaceus

Erythema toxicum neonatorum -24-72 hr after birth; lasts 1 wk Blotchy erythema with small central pustule; generalized, except palms and soles; full-term, healthy infants Clinical; Gram stain: eosinophils

Infantile acropustulosis Days to months; may last 2-3 yr Extremely pruritic vesicles and pustules occurring in crops on hands and feet Clinical; biopsy Eosinophilic

Miliaria (rubra or crystallina) Days to months; lasts hours to days Small erythematous papules (rubra) to clear vesicles (crystallina) on forehead, upper chest, and back; history of fever, overheating Clinical; all stains negative

Neonatal acne -Weeks to months Erythematous papules and pustules on face and chest; healthy neonates Clinical; stains mostly negative, but may see yeast forms

Transient neonatal pustular melanosis Birth; Pustules without erythema; collarette when wiped away; heals, but hyperpigmentation lasts generalized, palms, and soles; healthy neonates; more common in darker pigmented skin Gram stain: neutrophils

Congenital Syphilis Birth Vesicles and bullae, often eroded; snuffles, hands, and feet; may be localized or generalized; associated with hepatosplenomegaly and pseudoparalysis Serology; DFA; darkfield examination

VaricellaLinear scarring, erosions; often affects extremities; fetal anomalies occur with first- or secondtrimester infection Tzanck, DFA, PCR, culture, or serology

Herpes simplex Birth to weeks Vesicles or pustules; erosions to scarring; localized to generalized Tzanck, DFA, PCR, culture, or serology

Candidiasis, Erythematous macules or papules with satellite pustules; diaper area and flexures most commonly affected KOH: pseudohyphae

Staphylococcal scalded skin syndrome Painful erythema with localized flaccid bullae; may generalize to erythroderma; patient is ill appearing, with malaise, fever; Nikolsky sign positive; neonates most susceptible; caused by staphylococcal exfoliative toxins Clinical; cultures from mucosal surfaces and blood

Incontinentia pigmenti Birth Linear and whorled vesicles along lines of Blaschko; progresses to verrucous lesions; localized to limb or generalized; may be associated with seizures, retinopathy, and eosinophilia

Epidermolysis bullosa Birth to teens Noninflammmatory vesicles, bullae; often eroded extremities most often affected; severity depends on type; some forms associated with pyloric atresia, GI involvement, failure to thrive Biopsy; electron microscopy; genetic testing (keratins 5/14, plectin, laminin 5, collagen XVII, 64

Neonatal pemphigus Birth; resolves in a few weeks Pruritic, urticarial plaques with flaccid bullae, erosions; occurs in infants of mothers with active pemphigus vulgaris or foliaceus due to transfer of maternal antibodies Maternal history; biopsy; direct and indirect immunofluorescence

Porphyrias congenital erythropoietic porphyria, porphyria cutanea tarda, variegate porphyria) All may have varying degrees of photosensitivity with blistering; severe types present early, porphyria cutanea tarda in childhood Biopsy; porphyrin testing

Phototoxic Erythematous macules or papulovesicles with vesicle or bulla formation in photodistribution Clinical; biopsy

Dermatitis herpetiformis Intensely pruritic papulovesicles to vesicles; symmetrical over extensor surfaces; often associated with gluten-sensitive enteropathy Biopsy with immunofluorescence

Bullous pemphigoid Urticarial plaques with overlying tense bullae; may be annular or polycyclic; facial and palmar or plantar involvement more common in children Biopsy with direct and indirect immunofluorescence

Pemphigus vulgaris Generalized flaccid, easily eroded, crusted bullae; Nikolsky sign positive; may be drug induced Biopsy with direct and indirect immunofluorescence

Erythematous rash Possible diagnoses: psoriasis or pityriasis rosea. Psoriasis Pityriasis rosea Arthropod bites Erythema toxicum Milia Erythema multiform Steven johnson syndrome Acute sunburn reaction

PsoriasisFour variants of psoriasis are recognized: plaque, guttate, pustular, and erythrodermic. Infectious complications of psoriasis, such as cellulitis or sepsis, are conditions that warrant admission. Topical treatments may include topical steroids or topical steroid-sparing agents (e.g., tar). Thick scaling, especially of the scalp, may improve with applications of olive oil or over-the-counter tar shampoos. Phototherapy with ultraviolet light is effective for moderate to severe psoriasis. Severe or recalcitrant psoriasis may require systemic therapy and is best managed in conjunction with a specialist in dermatology.

Pityriasis rosea Papulosquamous eruption of school-aged children with small, red oval plaques with fine scales often aligned parallel to skin tension lines In 2080% , the generalized rash is preceded for up to 30 days by a single larger scaly plaque with central clearing (herald patch) often on the trunk (in whites) or extremities (in blacks) Human herpes virus 7 may be a pathogen Lasts about 6 weeks with mild-moderate pruritus History and visual diagnosis are key. Biopsy

Erythema nodosum Reactive inflammation of subcutaneous fatty tissue causing single

or multiple tender red/violaceous lumps usually over the shins. Resolving nodules look bruised Occurs in isolation but often after medications (oral contraceptive pills, estrogens, sulfa), infections (strep throat, Yersinia, tuberculosis, mycoplasma, cat scratch, fungal infections, Epstein-Barr virus, inflammatory bowel disease, autoimmune hepatitis Resolution usually occurs in 6 weeks but chronic/recurrent disease occurs Visual diagnosis usually sufficient. Biopsy showing septal inflammation in fatty layers is diagnostic

Erythema multiforme Targetoid to bullous erythematous macules or maculopapules; palms, soles, mucous membranes frequently affected; HSV most common trigger Clinical; biopsy

Stevens-Johnson syndrome & toxic epidermal necrolysis Generalized erythematous macules to morbilliform eruption frequent progression to flaccid bulla formation and widespread desquamation; mucosal involvement common; drugs, infections, vaccinations may trigger Clinical; biopsy

Drug eruptions majority are benign and self-limited. A subset of drug-associated rashes can be serious and even life threatening. Drug reactions result from both immunologic (e.g., IgE or T cell mediated) and nonimmunologic (e.g., cumulative toxicity, drug-drug interactions, or idiosyncrasy) mechanisms The drug hypersensitivity syndrome (DRESS) refers to a subset of severe drug reactions characterized by the triad of cutaneous eruption, fever, and internal organ dysfunction associated with exposure to a drug. Dramatic facial swelling is often seen, and patients are generally quite ill. There is a 10% mortality rate, with fulminant hepatic failure being the most common cause of death. Drug-induced vasculitis, drug-induced lupus, and serum sickness

A fixed drug eruption presents as a distinct lesion or lesions after systemic drug exposure. This eruption generally appears as sharply circumscribed, round to oval patches or plaques that may be single or multiple . The lesions are usually asymptomatic or only mildly pruritic. The eruption typically develops within 1 to 2 weeks of starting a new medication. The lesions may be red, gray, violaceous, or brown, and a central vesicle or bullae may be present. They tend to progress from erythematous to hyperpigmented. The rash may occur anywhere on the body, but the most common locations are the face, lips, hands, feet, and genitalia. A classic characteristic of a fixed drug eruption is that when patients are rechallenged with the offending medication, the lesion reappears in the same anatomic location and tends to appear much more rapidly, even within hours of taking the medicationThe most common agents implicated in fixed drug eruptions include sulfonamides, tetracyclines, nonsteroidal anti-inflammatory drugs (NSAIDs), barbiturates, and carbamazepine,

Fixed Drug Eruption

Eczematous rash Possible diagnoses: irritant contact dermatitis, allergic contact dermatitis, atopic dermatitis, or seborrhoeic dermatitis. Irritant dermatitis Nappy rash can result from direct irritation by stool or urine. Allergic contact dermatitis Atopic dermatitis

Atopic dermatitis Clinical Features of Atopic Dermatitis Essential Features Pruritus Eczema (acute, subacute, chronic)typical morphology and age-specific patterns with chronic or relapsing history Important Features Early age of onset Atopymanifested by personal or family history or immunoglobulin E reactivity Associated Features Atypical vascular responses dermatographism, delayed blanch response, facial pallor Keratosis pilaris, hyperlinear palms, ichthyosis Ocular or periorbital changes Other areas of change (e.g., periorbital, periauricular) Perifollicular accentuation, lichenification, prurigo lesions

Contact dermatitis (contact eczema) consists of patterned areas of erythema, scaling, oozing, or frank vesiculation. Linear or geometric areas may be noted in response to an allergen (e.g., poison ivy, nickel, fragrances).

Allergic contact dermatitis Very pruritic; may be localized or generalized; erythematous papulovesicles to bullae; linear distribution with poison ivy Clinical; biopsy

Seborrheic dermatitis seborrheic eczema is a salmon-colored erythema and scaling of the scalp, perinasal area eyebrows, ears, axillae, or diaper area; often, little pruritus is observed.

Dyshidrotic eczema Erythematous papulovesicles to bullae on hands and feet; may have generalized reaction Clinical; biopsy

Maculopapular rash Possible diagnoses: tinea corporis, scabies, second stage of impetigo, folliculitis, mastocytosis.

Impetigo Honey-colored, crusted, oozing vesicles with erythema; may be primary infection (common in perioral, perinasal regions) or secondary infection (atopic dermatitis, varicella); caused by Staphylococcus, Streptococcus, or both Clinical; Gram stain, culture

ScabiesVesicles to crusted papules, nodules with burrows; hands, feet, axilla, scalp Mineral oil preparation

diagnosis is clinical, and tests are not routinely recommended. laboratory investigations may be appropriate in patients in whom the cause is not clear. a rash suspected to be caused by a drug, no laboratory tests to determine or confirm the responsible drug are readily available

Investigations In suspected infectious aetiologies, bacteriology (e.g., Gram stain and/or culture of lesional fluid) may be prudent when the diagnosis is in doubt or if the patient does not respond to appropriate empirical therapy. Serum IgE levels, skin prick testing, and patch testing may be helpful in confirming a cause of allergic contact or atopic dermatitis. [43] Skin biopsy may be considered if a diagnosis of psoriasis, pityriasis rosea, or mastocytosis are considered.

FBC may show only mild to moderate peripheral eosinophilia. Metabolic, hepatic, and renal function panels are usually normal viral exanthema, depending on the particular virus involved, may need to be confirmed by serologically demonstrable antibody titres, viral culture, or molecular studies