Differentials
Common
Impetigo
History
children; 2 forms: bullous and nonbullous (more than 70% of cases nonbullous);[1] usually starts in a traumatized area
Exam
begins as an erythematous papule, then becomes a unilocular vesicle; when subcorneal vesicle becomes pustular, it ruptures and eventually becomes a yellow, golden crust (hallmark of disease process);[1] affects exposed areas, e.g., face and extremities; in bullous form, blisters usually less than 3 cm in diameter[2]
1st investigation
- none:
clinical diagnosis
Other investigations
- Gram stain:
neutrophils with gram-positive cocci in chains or clusters
- skin bacterial culture:
Staphylococcus aureus most commonly found, Streptococcus pyogenes or other group A beta-hemolytic streptococci
Folliculitis caused by Pseudomonas
History
history of exposure to contaminated water in hot tubs, swimming pools, saunas, and hydrotherapy pools that are underchlorinated[4]
Exam
multiple small papules and pustules on erythematous base, on any hair-bearing site, deeper infection resulting in follicular-centered dermal abscesses; 2- to 10-mm follicular papules, vesicles, and pustules, may be crusted, mostly seen in areas of the body that have been immersed in the contaminated water[78]
1st investigation
- Gram stain:
gram-negative rods
Other investigations
- skin bacterial culture:
Pseudomonas species
Folliculitis caused by Staphylococcus aureus
History
may begin with trauma to the skin, lesions typically resolve spontaneously
Exam
multiple small papules and pustules on erythematous base, on any hair-bearing site, with deeper infection resulting in follicular-centered dermal abscesses; inflammation manifests as 1-mm-wide vesicles, pustules, or papulopustules in acute cases but hyperkeratosis and keratotic plug formations indicate chronic process;[82] heal without scarring, hair shaft often seen in center of pustule; multiple or single lesions can appear on any hair-bearing skin including head, neck, trunk, buttocks, and extremities; deep folliculitis presents with swelling and erythema with or without pustule at skin surface, and these lesions are painful and may scar[4]
1st investigation
- none:
clinical diagnosis
Other investigations
- Gram stain:
gram-positive cocci
- skin bacterial culture:
S aureus species
- nasal bacterial culture:
S aureus colonization
Pityrosporum folliculitis
History
incidence can be associated with either immunosuppressive or chemotherapy treatment; more prevalent in hot and humid climates[73]
Exam
1st investigation
- KOH preparation:
dermatophyte infections show hyphae; Pityrosporum yeast show hyphae and spores
Other investigations
- skin fungal culture:
dermatophyte infections: Pityrosporum yeast
Herpes simplex virus
History
reactivation of virus can be spontaneous or triggered by factors such as fever, UV light exposure, common cold, emotional stress, fatigue, trauma; primary infection with HSV-1 mainly causes gingivostomatitis (oral infection with HSV-2 is also unusual);[64] pain is a typical symptom
Exam
initial vesicular rash; lesions appear as erythematous papules that turn into grouped vesicles and latterly pustules eventuating into crusts[81]
1st investigation
- DNA analysis via PCR:
positive for HSV
Other investigations
- Tzanck smear:
multinucleated giant cells, epithelial cells with eosinophilic intranuclear inclusion bodies
- direct immunofluorescence study:
positive for HSV
- skin viral culture:
positive for HSV
- skin biopsy:
epithelial cells with intranuclear eosinophilic inclusion bodies; leukocytoclastic vasculitis and hemorrhage
Dermatophytosis: tinea barbae
History
involves skin and coarse hairs of beard and mustache area; occurs in adult men and hirsute women; farm workers are most often affected because the usual cause is a zoophilic organism[77]
Exam
scaling, follicular pustules, and erythema[77]
1st investigation
- KOH preparation:
hyphae
Other investigations
- skin fungal culture:
positive for specific dermatophytes
- skin biopsy:
periodic acid-Schiff positive for hyphae
Dermatophytosis: tinea cruris
History
patients frequently complain of burning and pruritus[15]
Exam
affects proximal medial thighs and may extend to buttocks and abdomen; scrotum tends to be spared;[15] pustules and vesicles at active edge of infected area, along with maceration, are present on a background of red, scaling lesions with raised borders
1st investigation
- KOH preparation:
hyphae
Other investigations
- skin fungal culture:
positive for specific dermatophytes
- skin biopsy:
periodic acid-Schiff positive for hyphae
Dermatophytosis: tinea pedis
History
presents with fungal maceration, and fissuring
Exam
vesiculobullous form of tinea pedis is characterized by development of vesicles, pustules, and sometimes bullae in an inflammatory pattern, usually on the soles[15]
1st investigation
- KOH preparation:
hyphae
Other investigations
- skin fungal culture:
positive for specific dermatophytes
- skin biopsy:
periodic acid-Schiff positive for hyphae
Dermatophytosis: tinea corporis
History
presents on trunk, extremities, or face;[79] itching varies
Exam
single or multiple, annular, scaly lesions with central clearing, slightly elevated reddened edge and sharp margination (abrupt transition from abnormal to normal skin) on trunk, extremities, or face; lesion border may contain pustules or follicular papules[15]
1st investigation
- KOH preparation:
hyphae
Other investigations
- skin fungal culture:
positive for specific dermatophytes
- skin biopsy:
periodic acid-Schiff positive for hyphae
Acne vulgaris
History
irregular menses, increased weight, diabetes and/or hirsutism may point to androgen excess, resulting in acne lesions; congenital adrenal hyperplasia, PCOS, and other endocrine disorders with excess androgens may trigger development of acne vulgaris;[72] certain medications can promote acne (corticosteroids, lithium, some antiepileptics and iodides)[19]
Exam
moderate acne is characterized by comedone formation but also moderate numbers of papules and pustules, formed following the rupture of comedones and subsequent Propionibacterium acnes proliferation and inflammation; moderately severe acne is composed of more numerous papules, pustules, and comedones as well as a few nodular lesions affecting the face, chest, and back; severe or nodulocystic acne has many painful nodular lesions as well as smaller papules, pustules, and comedones[83]
1st investigation
- none:
diagnosis is clinical
Other investigations
- free testosterone (female patients):
may be elevated in PCOS; significantly elevated in androgen-secreting tumor
- dehydroepiandrosterone sulfate (female patients):
may be normal or slightly elevated in PCOS; significantly elevated in androgen-secreting tumor
- LH (female patients):
may be normal or elevated in PCOS
- FSH (female patients):
may be elevated in primary ovarian failure
Eosinophilic folliculitis (Ofuji syndrome/disease)
History
Exam
multiple small papules and pustules on erythematous base, on any hair-bearing site, with deeper infection resulting in follicular-centered dermal abscesses; classic form: chronic and recurrent annular clusters of sterile follicular papules and pustules superimposed on plaques with central clearing and peripheral extension; individual clusters last for 7 to 10 days and tend to relapse every 3 to 4 weeks; immunosuppression-associated form: pruritic discrete erythematous raised follicular papules[21]
1st investigation
- histology of skin biopsy:
eosinophilic folliculitis shows eosinophils and lymphocytes within the hair follicle
Other investigations
- CBC:
eosinophilic folliculitis: leukocytosis and eosinophilia
- IgE:
elevated
Subcorneal pustular dermatosis (Sneddon-Wilkinson disease)
History
benign, chronic, recurrent, sterile vesiculopustular eruptions involving flexural areas of the trunk and proximal extremities; history of immunoglobinopathies and lymphoproliferative disorders, e.g., IgA multiple myeloma; also associated with CD30+ anaplastic large cell lymphoma, non-small cell lung cancer, apudoma, rheumatoid arthritis, hyperthyroidism, and Mycoplasma pneumoniae infection[27]
Exam
lesions coalesce into annular, circinate, or serpiginous patterns, preferring trunk and intertriginous areas (axillae, groin, and submammary regions); pustular dermatosis type IgA pemphigus: distribution of subcorneal lesions can be widespread and involve scalp and face, locations usually spared in classic subcorneal pustular dermatosis[27]
1st investigation
- skin biopsy:
subcorneal pustule filled with PMN leukocytes; underlying epidermis is generally spared, demonstrating minimal spongiosis or acantholysis
Other investigations
- serum protein electrophoresis:
IgA monoclonal gammopathy (kappa or lambda light chain type); occasional IgG gammopathy
- immunofluorescence:
positive immunofluorescence of IgA restricted to upper epidermis in pustular dermatosis type IgA pemphigus
Infantile acropustulosis (IA)
History
condition of young children characterized by recurrent episodes of pruritic vesicles and pustules in an acral distribution; possibly recent history of scabies[29]
Exam
1st investigation
- CBC:
eosinophilia
Other investigations
- skin biopsy:
subcorneal, or intraepidermal pustule containing PMN neutrophils or eosinophils
More
Fire ant bites
History
bites result in immediate severe burning and itching at the sting sites[32]
Exam
localized hive develops at sting site within 20 minutes, followed by a necrotic lesion, termed the sterile pustule, which lasts for several days[32]
1st investigation
- none:
clinical diagnosis
Other investigations
- skin testing:
confirms fire ant hypersensitivity
- ELISA:
confirms fire ant hypersensitivity
- RAST:
confirms fire ant hypersensitivity
Acrodermatitis continua (pustular acrodermatitis, acrodermatitis continua suppurativa Hallopeau, dermatitis perstans, and dermatitis repens Crocker)
History
begins on 1 digit, but other digits may become involved during chronic course of the disease; intermittent pustulations may lead to atrophy, onychodystrophy, and even osteolysis[39]
Exam
1st investigation
- skin biopsy:
acanthosis, papillomatosis, and perivascular infiltration of lymphocytes and neutrophils in upper dermis with partial migration to epidermis
Other investigations
Pustular drug rash secondary to epidermal growth factor receptor (EGFR) inhibitors
History
history of colorectal or non-small cell lung cancer treated with EGFR inhibitors (cetuximab, erlotinib, gefitinib), onset between 1 to 3 weeks of treatment, possibly waxing and waning, may be associated with mild pruritus
Exam
lesions are similar to acne vulgaris, with a predominance of pustules and no associated comedones; monomorphous erythematous maculopapular, follicular or pustular lesions; commonly affects face (nose, cheeks, nasolabial folds, chin, forehead), areas of the upper chest and/or back[43]
1st investigation
- skin biopsy:
2 major patterns: 1) moderate superficial dermal inflammatory cell infiltrate surrounding hyperkeratotic and ectatic follicular infundibula, particularly in upper portion of hair follicle; 2) superficial neutrophilic suppurative folliculitis with associated rupture of epithelial lining
Other investigations
Acute generalized exanthematous pustulosis (AGEP)
History
often a female patient with exposure to antimicrobials (commonly aminopenicillins and macrolides), diltiazem, sulfonamides, terbinafine, quinolones, acetaminophen, progesterone preparations, mercury; may occur soon or 1 to 2 weeks after exposure; rash lasting 6 to 31 days followed by desquamation[68][69]
Exam
1st investigation
- skin biopsy:
spongiform subcorneal pustule, edema of papillary dermis, perivascular infiltrate of neutrophils
Other investigations
- CBC:
leukocytosis, with WBC counts over 10,000/microliter
- bacteriologic culture studies:
usually negative
- metabolic panel:
transient renal failure, hypocalcemia
- rechallenge with the suspected drug:
positive
- patch testing:
positive
- interferon-gamma release assay:
positive
More - in vitro test: macrophage migration inhibition factor test:
positive
- in vitro test: mast cell degranulation test:
positive
Generalized pustular psoriasis (von Zumbusch type)
History
sudden eruption (within a few hours) of generalized sterile pustules; may have a family history of psoriasis and/or history of drug administration; history of impetigo herpetiformis in prior pregnancy; history of trigger factors (infections [e.g., URTI], drugs [e.g., corticosteroid withdrawal] coal tar, iodides and minocycline, pregnancy, hypocalcemia, and hypoparathyroidism); pustules usually erupt in waves with recurrent bouts of fever, arthralgias and myalgias; trunk, extremities, palms, soles, and nail beds are commonly involved and the face is usually spared[50]
Exam
pustules usually on an erythematous base 2 to 3 mm in diameter; pustules may coalesce into larger lakes of pus; can progress to erythroderma
1st investigation
- histology of skin biopsy:
spongiform neutrophilic pustules, parakeratosis, elongated rete ridges and mononuclear infiltrates in dermis
Other investigations
- metabolic panel:
hypocalcemia
- CBC:
absolute lymphopenia with PMN leukocytosis
- ESR:
elevated
Transient neonatal pustular melanosis
History
most common in black people; occurs predominantly on forehead, back, posterior neck, and shins; 3 distinct clinical phases[33]
Exam
first, superficial, 2- to 10-mm vesiculopustules without inflammation are present at or near birth; lesions usually clear within the first week, and the second phase becomes apparent as a collarette of fine scale develops around the resolving vesiculopustules; last, macules of brown hyperpigmentation develop at the sites and eventually fade over the first few weeks to months[33]
1st investigation
- Gram/Giemsa stains:
neutrophils without evidence of bacteria, yeast, or viropathic changes
Other investigations
- culture:
sterile
Pustulosis palmaris et plantaris (PPP)
History
chronic, relapsing inflammatory disease characterized by multiple pustules and erythematous plaques on palms and soles; focal infection, such as tooth infection or tonsillitis, is a well-known exacerbating factor of PPP[76]
Exam
3 steps are evident during the exacerbation of PPP: first vesicles, then vesiculopustules and finally pustules; in very early lesions, erythema appears, then vesicles and pustules occur in erythematous patches[76]
1st investigation
- skin biopsy:
early lesions of vesicles histologically show basal epidermal spongiosis around tip of dermal papillae, then pustules show subcorneal blisters, finally contents of pustules consist of PMN leukocyte infiltrations
Other investigations
Erythema toxicum neonatorum
History
acute, self-limiting skin manifestation that develops in 50% to 70% of all healthy newborn infants, particularly those born at term; starts soon after birth and disappears spontaneously within a few weeks without sequelae[30]
Exam
papulopustules on an intense erythematous base[30]
1st investigation
- none:
clinical diagnosis
Other investigations
- Tzanck smear and Gram stain:
inflammatory cells: greater than 90% eosinophils and some neutrophils
- CBC:
eosinophilia
- skin biopsy:
dense inflammatory infiltrate around hair follicles, composed mostly of eosinophils, but also containing neutrophils, macrophages, and dendritic cells
Uncommon
Gram-negative folliculitis
History
occurrence of gram-negative folliculitis should be considered in acne patients without significant improvement of acne lesions after 3 to 6 months' treatment with oral tetracyclines[5]
Exam
lesions limited to the face and consist either of superficial small pustules located in the nasolabial line and on the upper lip and chin, associated with inflammatory papulopustular lesions of the cheeks and perioral region, or of deeply sited and painful nodules of the cheeks[80]
1st investigation
- skin culture:
gram-negative bacteria (lactose-fermenting gram-negative rod group)
Other investigations
Folliculitis caused by herpes and other viruses
History
Exam
multiple small papules and pustules on an erythematous base, on any hair-bearing site, with deeper infection resulting in follicular-centered dermal abscesses; lesions appear as erythematous papules, vesicles or pustules are rare[75]
1st investigation
- Tzanck smear:
multinucleated giant cells, epithelial cells with eosinophilic intranuclear inclusion bodies
Other investigations
- skin viral culture:
HSV or herpes zoster
Secondary syphilis
History
rash develops 6 to 10 weeks after resolution of the painless chancre; patients present with a variety of symptoms, such as malaise, sore throat, headache, weight loss, low-grade fever, pruritus, and muscle aches, in addition to dermatologic manifestations[6]
Exam
painless coin-like macular lesions on flank, shoulders, arms, chest, back, hands, and soles of feet; lesions typically reddish brown and 3 to 10 mm in size; variations of secondary syphilis skin eruptions may include pustules; other associated lesions include patchy (moth-eaten) alopecia, genital lesions (condylomata lata), superficial mucosal erosions (mucous patches)[6]
1st investigation
- VDRL:
antilipoidal antibodies
- RPR:
antilipoidal antibodies
Other investigations
- darkfield microscopy:
direct visualization of organism
- FTA-ABS test:
detects antibodies to treponemes
- microhemagglutination assay for Treponema pallidum:
detects antibodies to treponemes
- histology of skin biopsy:
cellular infiltrate consists primarily of lymphocytes, plasma cells, macrophages, some PMN leukocytes, epithelioid cells, and occasional giant cells
Infantile scabies
History
scabies should be suspected in infants or children with generalized pruritus of recent onset and characteristic eruption; site, severity, duration and timing of itch are all useful in diagnosis; nocturnal itch is very characteristic; history of itching in other family members should be sought and may help diagnosis;[16] atypical distribution, absence of burrows and eczematization are important reasons for low suspicion
Exam
classical eruption of scabies presents as pruritic papules, vesicles, pustules, and linear burrows; most patients only have an admixture of the primary lesions along with excoriations, eczematization, crusting, and secondary infection; pathognomonic scabies burrow is an elevated white and serpiginous tract 0.3 to 0.5 mm by 10 mm long; excoriations, crusting, and eczematization may completely obscure these and any other primary lesion[16]
1st investigation
- microscopic mineral preparation:
presence of Sarcoptes scabiei mites, eggs, or feces (scybala)
Other investigations
Candidal infection and disseminated candidiasis
History
risk factors includeCandida colonization, treatment with broad-spectrum antibiotics, central venous catheter, parenteral nutrition, GI or cardiac surgery, prolonged hospital stay, ICU stay, burns, necrotizing pancreatitis, dialysis, premature birth, immunosuppression (neutropenia, corticosteroid treatment, HIV infection, DM);[12] congenital candidiasis: acquired in utero and presents at birth or within the first few days of life;[67] neonatal candidiasis: development of mucocutaneous Candida infection after the first few days of life, acquired during or after delivery; resembles Candida skin infections in older infants[67]
Exam
congenital cutaneous candidiasis: monilial diaper dermatitis, or diffuse, erythematous, papulopustular eruption with scaling and widespread erosions, or a burnlike dermatitis; concomitant thrush is not commonly seen; palms and soles may be involved, and onychomycosis and paronychia have been reported;[67] neonatal candidiasis: erythematous patches with peripheral papules and pustules, and scaling in intertriginous areas, including diaper area, inguinal creases and perianal area, is typical[67]
1st investigation
- KOH preparation:
hyphae, pseudohyphae, and budding yeast forms
- Gram stain:
hyphae, pseudohyphae, and budding yeast forms
Other investigations
- skin yeast culture:
positive for Candida species
- blood cultures:
positive for Candida species in disseminated candidiasis
- serologic 1,3 beta-glucan assay:
positive for beta-glucan antibodies
More
Perioral dermatitis
History
overhydration of skin caused by frequent use of occlusive moisturizing emollients leads to irritation and impairment of skin barrier function; atopic disposition is quite often found; abuse of topical corticosteroids can be another triggering factor in some cases;[74] patients report burning rather than itching[74]
Exam
erythematous papules or papulopustules, usually not larger than 2 mm; frequently accompanied by diffuse erythema and scaling; although perioral is the most frequent location, periocular areas, nasolabial folds, and glabella may also be affected[40]
1st investigation
- none:
clinical diagnosis
Other investigations
Behcet disease
History
occurs around the third decade of life and has a chronic course with unpredictable exacerbations and remissions; characterized by oral aphthae and by at least 2 of the following: 1) genital aphthae, 2) synovitis, 3) posterior uveitis, 4) cutaneous pustular vasculitis, 5) meningoencephalitis, 6) recurrent genital ulcers, 7) uveitis in the absence of inflammatory bowel disease or collagen vascular disease[23]
Exam
papulopustular lesions are the most common skin lesions: sterile, folliculitis or acne-like lesions on an erythematous base that appear as a papule initially and then evolves into a pustule over 24 to 48 hours; patients may also exhibit pathergy (new lesions develop at sites of trauma)[88]
1st investigation
- skin biopsy:
variable, depending on type of lesion: early papulopustular lesions show leukocytoclastic vasculitis with neutrophilic infiltrate, extravasated RBCs, and fibrinoid necrosis within vessel walls
Other investigations
Pseudofolliculitis barbae
History
history of shaving or tweezing affected area[26]
Exam
papules and pustules that appear in the beard distribution are the most common presentation; anterior neckline, mandibular areas, cheeks, and chin are the most common sites[26]
1st investigation
- histology of skin biopsy:
mononuclear leukocytes and PMN leukocytes in pustules; mononuclear leukocytes and PMN leukocytes as well as micrococci in papules
Other investigations
- cultures:
usually sterile or containing normal skin flora
Neonatal cephalic pustulosis (neonatal acne)
History
may be present at birth, but more frequently appears at 2 to 3 weeks of age and resolves spontaneously; benign cephalic pustulosis is differentiated from infantile acne by its lack of comedonal lesions and earlier onset[33]
Exam
characterized by small, inflammatory, erythematous papules and pustules found on the cheeks, forehead, and scalp[33]
1st investigation
- none:
clinical diagnosis
Other investigations
- Tzanck smear:
inflammatory cells: greater than 90% eosinophils and some neutrophils in erythema toxicum neonatorum
More - direct microscopy of KOH preparations:
positive in candidal folliculitis
More - Gram stain:
positive for hyphae in candidal folliculitis or bacteria in bacterial folliculitis
More - skin bacterial cultures:
positive in bacterial folliculitis
More - skin yeast culture:
May be positive for Malassezia species
Miliaria rubra ("prickly heat")
Exam
1 to 3 mm erythematous, nonfollicular-based papules and papulopustules, usually on the forehead, upper trunk, and flexural or occluded areas[33]
1st investigation
- none:
clinical diagnosis
Other investigations
Pustular rosacea
History
persistent facial erythema, recurrent episodes of flushing, edema, papules, and pustules; later, telangiectasia, dermatitis, burning sensations, fibrosis, and ocular signs may occur[89]
Exam
characterized by facial flushing, erythema, telangiectasia, inflammatory episodes with papules and pustules, and, in severe cases, rhinophyma[36]
1st investigation
- none:
clinical diagnosis
Other investigations
Reactive arthritis
History
classically includes the triad of conjunctivitis, urethritis, and arthritis in young male patients after GI or urogenital infection; patients with reactive arthritis also manifest mucocutaneous symptoms: keratoderma blennorrhagicum, circinate balanitis, ulcerative vulvitis, nail changes, and oral lesions[38]
Exam
keratoderma blennorrhagicum begins as erythematous macules and vesicles typically on palms and soles, and progresses to pustules, papules, and hyperkeratotic plaques; can also occur on the trunk, scalp, extensor surfaces of legs, back of toes, and fingers[38]
1st investigation
- skin bacterial cultures:
associated enteric organisms include Shigella flexneri (types 2a and 1b), Salmonella typhimurium, Salmonella paratyphi, Salmonella cholerae, Salmonella suis, Salmonella enteritidis, Salmonella heidelberg, Yersinia enterocolitica, Yersinia pseudotuberculosis, Campylobacter fetus, Campylobacter jejuni, Clostridium difficile; associated urogenital organisms include Ureaplasma urealyticum, Chlamydia psittaci, Chlamydia trachomatis (D-K), and Neisseria gonorrhoeae
Other investigations
- plain x-ray of involved joints:
erosions with indistinct margins surrounded by periosteal new bone, asymmetric, oligoarticular joint involvement
- skin biopsy:
spongiform macropustule in upper epidermis, intraepidermal microabscesses, marked papillomatosis, acanthosis; older lesions show thickened cornified layer and acanthosis
- joint aspiration:
macrophages with vacuoles filled with nuclear debris and whole leukocytes
Drug rash with eosinophilia and systemic symptoms (DRESS)
History
characterized by acute drug-induced eruption, fever, lymphadenopathy, and/or internal organ involvement; starts within 8 weeks after initiation of therapy;[46] skin is the most commonly involved organ in DRESS, with a very wide spectrum of manifestations and severity; hematologic abnormalities, especially eosinophilia and mononucleosis-like atypical lymphocytosis, are also common;[46] medication history including carbamazepine, phenytoin, phenobarbital, zonisamide, mexiletine, dapsone, sulfasalazine and allopurinol, sulfonamides, allopurinol, gold salts, dapsone and minocycline
Exam
morbilliform eruption usually found initially; face, upper trunk, and upper extremities are affected first with later involvement of lower extremities;[46] vesicles and tight blisters; sterile follicle-centered pustules may exist, as well as nonfollicular small pustules; erythroderma may occur; edema of the face, often more marked in periorbital regions; mucosal involvement, such as cheilitis, erosions, erythematous pharynx, and enlarged tonsils; fever, lymphadenopathy, and clinical features of severe visceral involvement like hepatitis, nephritis, pneumonitis, and/or myocarditis; thyroiditis has been reported to develop in a small subset of patients
1st investigation
- skin biopsy:
dense lymphocytic infiltrate in superficial dermis and/or perivascularly, associated with eosinophils and dermal edema; occasional atypical lymphocytes
Other investigations
- CBC:
eosinophilia is seen in 60% to 70% of patients, mononucleosis-like atypical lymphocytosis in the circulation
- LFTs:
possibly elevated secondary to hepatitis
- serum creatinine level:
elevated
- urinalysis:
proteinuria, abnormal urinary sediment with occasional eosinophils indicating interstitial nephritis
- TSH:
may be elevated or low secondary to thyroiditis
- chest x-ray:
lung lesions consist of interstitial and alveolar infiltration by lymphocytes and eosinophils
Corticosteroid-induced rosacea-like eruption/corticosteroid acne
History
may occur after administration of topical or systemic corticosteroids; lesion onset weeks or months after initiation of corticosteroid therapy;[70] manifestation of corticosteroid dermatitis depends on potency of corticosteroids, body area and duration of their activity;[70] withdrawal of topical corticosteroids may lead to rebound of previous corticosteroid-responsive facial dermatoses[48]
Exam
topical corticosteroids cause local reaction (corticosteroid rosacea), characterized by presence of nontransient erythema, papules and pustules, telangiectasias with burning or stinging sensation, and dry appearance;[48] systemic corticosteroids can result in minute, monomorphous, erythematous papules and pustules on upper trunk, often sparing the face; comedones are generally absent with both types of reactions[70]
1st investigation
- none:
clinical diagnosis
Other investigations
Ulcerative or typical pyoderma gangrenosum
History
multiple lesions, with lower extremity the most common site of involvement; pathergy occurs in 20% to 30% of patients, and severe exacerbations may occur after physical trauma such as debridement, which is contraindicated[53]
Exam
cutaneous lesions begin as tender papules, papulopustules, or vesicles that develop into painful ulcers with ragged, overhanging, dusky purple edges and surrounding induration and erythema; ulcer bases may contain granulation tissue, necrotic tissue and/or purulent exudate; lesions heal with atrophic, cribriform scars[53]
1st investigation
- skin biopsy:
early lesions reveal neutrophilic vascular reaction pattern (may be folliculocentric); fully developed ulcers exhibit marked tissue necrosis with surrounding mononuclear cell infiltrates
- skin bacterial cultures:
bacteria, atypical mycobacteria infection of ulceration
- skin viral cultures:
viral infection of ulceration
- skin fungal cultures:
fungal infection of ulceration
Other investigations
- hepatitis profile:
positive in hepatitis
More - serum and/or urine protein electrophoresis:
evidence of hematologic malignancies
- peripheral blood smear:
evidence of hematologic malignancies
- bone marrow aspiration:
evidence of hematologic malignancies
- flexible sigmoidoscopy and biopsy:
excludes associated inflammatory bowel disease such as ulcerative colitis
Atypical form of pyoderma gangrenosum (APG)
History
mean age of onset is 52.2 years (ranging from 37 to 67 years)[53]
Exam
lesions may resemble those of Sweet syndrome, both clinically and histopathologically, but APG ulcerates and heals with scarring;[53] sweet-like painful, blue-gray inflammatory bullae that erode or superficially ulcerate and are most commonly located on the upper extremities
1st investigation
- skin biopsy:
early lesions reveal neutrophilic vascular reaction pattern (may be folliculocentric); fully developed ulcers exhibit marked tissue necrosis with surrounding mononuclear cell infiltrates; APG biopsy specimens exhibit the same features as typical pyoderma gangrenosum specimens but are located more superficially in the dermis; spongiosis and vesiculation may also be present
- hepatitis profile:
positive in hepatitis
More - serum and/or urine protein electrophoresis:
evidence of hematologic malignancies
- peripheral smear:
evidence of hematologic malignancies
Other investigations
- bone marrow aspiration:
evidence of hematologic malignancies
- skin bacterial cultures:
bacteria, atypical mycobacteria infection of ulceration
- skin viral cultures:
viral infection of ulceration
- skin fungal cultures:
fungal infection of ulceration
- flexible sigmoidoscopy and biopsy:
excludes associated inflammatory bowel disease such as ulcerative colitis
Orf
History
history of contact with lesions on animals (usually sheep or goats) or contaminated fomites[10]
Exam
solitary lesion typically on a finger or hand, and uncommonly on the face; lesions progress through 6 stages, each stage lasting approximately 1 week and include: 1) maculopapular stage: erythematous macule, papule or pustule, 2) target stage: formation of a central erythematous nodule with a middle white ring and an outer red halo, 3) acute stage: weeping nodule, 4) regenerative stage: black dots and a yellow crust, 5) papillomatous stage: verrucous nodule, 6) regressive stage: involution of the lesion[10]
1st investigation
- none:
clinical diagnosis
Other investigations
- skin biopsy:
depends on the clinical stage; first and second stages: pallor and vacuolization of cells in the epidermis, with intracytoplasmic and occasionally intranuclear inclusion bodies; acute stage: reticular degeneration of the epidermis, dilated hair follicles demonstrating cytopathic changes similar to those of earlier stages, and a mixed inflammatory infiltrate in the dermis; fourth stage: regeneration of the epidermis, with extrusion of follicular cells onto the surface; papillomatous stage: endophytic fingerlike projections of the epidermis; regressive stage: decrease in epidermal acanthosis with resolution of the inflammatory infiltrate[10]
Amicrobial pustulosis of the folds (APF)
History
relapsing pustular lesions predominantly involving the cutaneous flexures and scalp; typically in association with an autoimmune or connective tissue disease, including SLE, scleroderma overlap syndrome, discoid lupus erythematosus, sicca syndrome, celiac disease, idiopathic thrombocytopenia, or myasthenia gravis;[41][71] course is frequently chronic with recalcitrant relapses; usually no relation between course of the cutaneous lesions and activity of associated autoimmune disorder
Exam
cutaneous eruption consists of small follicular and nonfollicular sterile pustules, coalescing into erosive plaques; the lesions predominate in the cutaneous folds, the scalp, the genital area and the external auditory canal[41]
1st investigation
- skin biopsy:
light microscopy studies of pustular lesions reveal intraepidermal pustules and eosinophilic spongiosis; direct immunofluorescence studies, including the lupus band test, are negative
Other investigations
Erosive pustular dermatosis
History
sterile pustules on the scalp; may be preceded by trauma or may arise de novo; pustular component may mimic a bacterial infection[57]
Exam
chronic sterile pustules, erosions, and crusted lesions confined to the scalp (usually actinically damaged)
1st investigation
- skin biopsy:
histology should not show any other etiology for the sterile papular rash
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Other investigations
- Tzanck smear:
negative
- bacterial culture:
sterile
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