(1)
Division of Internal Medicine, Department of Dermatology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
Eczema
Differential Diagnosis of Pruritus
INFLAMMATORY
dermatitis—atopic dermatitis, asteatotic eczema, nummular eczema, dyshidrotic eczema, seborrheic dermatitis, stasis dermatitis, irritant contact dermatitis, allergic contact dermatitis, lichen simplex chronicus (neurodermatitis)
psoriasis
pityriasis lichenoides
urticaria
dermatitis herpetiformis
bullous pemphigoid
graft vs host disease
INFECTIONS
—tinea, scabies, pediculosis corporis and pubis, pityriasis rosea
NEOPLASTIC
—lymphoma (mycosis fungoides, Hodgkin lymphoma), myeloma, solid tumors, polycythemia vera
IATROGENIC
drug eruption—antibiotics, anti-epileptics
drug – induced pruritus—opiates, steroids, aspirin, antimalarials
SYSTEMIC
endocrine—diabetes, hypothyroidism, hyperthyroidism
hepatobiliary—PBC, cholestasis
renal—uremia, hemodialysis
neurologic—brachoradial pruritus, notalgia paresthetica, postherpetic neuralgia, multiple sclerosis, psychogenic itch
infections—HCV, HIV
others—sarcoidosis, iron deficiency
Pathophysiology
PATHOGENESIS
—chronic inflammatory skin disorder characterized by dry skin and pruritus. Rubbing and scratching the skin promotes inflammation and leads to an itch–scratch cycle. It follows a relapsing course characterized by alternating periods of flares and remissions. Patients often have a personal or family history of eczema, asthma, or allergic rhinitis. Exacerbating factors may include cold weather, dust mites, pollens, infection, wool, pet fur, emotional stress, chemical irritants, and other allergens
Clinical Features
FINDINGS
—ill-defined pruritic erythematous plaques with excoriations. Neck and flexural prominence in adults and children. Pustules, honey-colored crusts, and weeping may be a sign of secondary infection
TYPES OF ECZEMA
asteatotic eczema—dry irritable skin in the elderly
nummular eczema—acral, coin-shaped patches of eczema usually on extremities
dyshidrotic eczema—acute vesicular eczema of the palms and soles
xerosis / winter itch—eczema secondary to dry conditions in winter
Investigations
SPECIAL
(not typically performed)
labs—CBCD (eosinophilia) and IgE level (elevated)
bacterial and viral cultures—if there is a suspicion of a secondary infection
Management
TREATMENTS
—dry skin care (unscented, hypoallergenic soaps, daily moisturizers). Topical corticosteroids BID × 3 weeks, off 1 week, repeat PRN (typically hydrocortisone 1–2.5% or desonide 0.05% for the face, triamcinolone 0.1% for the body), and topical calcineurin inhibitors (tacrolimus 0.1%, pimecrolimus 1%). Antihistamines (diphenhydramine, loratadine, fexofenadine, hydroxyzine, and doxepin). Oral antibiotics × 7 days for superimposed Staphylococcus aureus infections (typically flucloxacillin or other penicillinase-resistant penicillin for MSSA and clindamycin, doxycycline or trimethoprim-sulfamethoxazole for MRSA)
Specific Entities
DERMATITIS HERPETIFORMIS
associations—Celiac disease, IgA nephropathy, autoimmune thyroid disease, autoimmune hepatitis, type 1 diabetes, SLE, Sjogren’s syndrome, sarcoidosis, Addison’s Disease, atrophic gastritis, vitiligo, and alopecia areata. Strong linkage to HLA-B8, DR3, and DQw2. Increased risk of non-Hodgkin’s lymphoma
clinical features—pruritic papulovesicles on extensor surfaces and buttocks, rarely mucous membranes. Lesions tend to be symmetrically distributed
treatments—dapsone and gluten-free diet. See Celiac disease (p. 139)
STASIS DERMATITIS
clinical features—erythematous pruritic and burning lesions found on lower limbs of older patients due to compromised venous or lymphatic return. With increased extravasation of blood into the surrounding tissues, the lesions become darker, scalier, and may even form stasis ulcers
treatments—treat underlying cause. Leg elevation. Graduated compression stockings (after ankle–brachial index [ABI] checked). Topical steroids for acute exacerbations. Varicose veins may be treated with surgery, endovenous laser therapy or via sclerotherapy
SCABIES
clinical features—excoriations, eczematized and urticarial papules over trunk. Linear white burrows over finger webs, sides of hand, and flexural aspects of wrists. Confirmed by skin scrapings for mites and eggs
treatments—first-line therapy with permethrin 5% cream × 1 dose, applied to the entire body from chin to soles, rinse off after 8–14 h. Second-line treatments include ivermectin 200 mcg/kg PO × 1 dose and repeat PO × 1 dose 2 weeks later, lindane 1% lotion or cream × 1 dose, rinse off after 8 h, and benzyl benzoate 10 or 25% lotions × 1 dose, rinse off after 24 h. Simultaneous treatment of patient and close contacts is recommended
NEJM 2006 354:16
Psoriasis Vulgaris
Differential Diagnosis of Papulosquamous Lesions
INFLAMMATORY
—psoriasis vulgaris, lichen planus, nummular eczema, discoid lupus
INFECTIONS
—tinea, pityriasis rosea, secondary syphilis, seborrheic dermatitis
MALIGNANCY
—mycosis fungoides, basal cell carcinoma (BCC), squamous cell carcinoma (SCC)
IATROGENIC
—drug eruption
Pathophysiology
INFLAMMATION
—a chronic inflammatory skin disorder with a polygenic predisposition and sometimes an environmental triggering factor (trauma/Koebner phenomenon, infections, drugs, alcohol ingestion, emotional stress)
Clinical Features
FINDINGS
—well-circumscribed, bright salmon red color, silvery micaceous scaly plaques. Predilection for the scalp and extensor regions. Nails may show pitting changes, “oil spots”, onycholysis, and subungual debris which may be helpful in making the diagnosis. All patients regardless of skin severity should be screened for inflammatory arthritis that is worse in the mornings, associated with joint stiffness and swelling ± dactylitis. Consider screening for hyperlipidemia, coronary artery disease, and diabetes in patients with risk factors as there is an increased predilection in patients with psoriasis
SUBTYPES
chronic plaque psoriasis—predilection for scalp, elbows, and knees. Symmetric, sharply demarcated erythematous plaques with silvery scales that when scratched off reveals punctate blood droplets (Auspitz sign)
guttate psoriasis—predilection for trunk. May follow a streptococcal infection. Multiple discrete erythematous papules with silvery scales
palmoplantar psoriasis—mild to severe forms. Well-demarcated erythematous plaque with silver scales. Cracking, fissures, or bleeding may be seen. Pustular variant also found
inverse psoriasis—perianal, genital, and axillary well-demarcated erythematous plaques that are more likely to be macerated and fissured due to location in a moist and warm environment
erythrodermic psoriasis—generalized erythema ± characteristic erythematous plaques with white-silver scale and nail changes. Often spares the face
pustular psoriasis—initial stinging and burning in area may promote scratching, followed by eruption of sterile pustules
Investigations
SPECIAL
(not typically performed)
microbiology—throat C&S (if guttate psoriasis)
KOH preparation—if suspect tinea
skin biopsy
Management
TREAT UNDERLYING CAUSE
—topical therapy with corticosteroids (triamcinolone/fluocinolone, fluocinonide, betamethasone dipropionate and clobetasol) and vitamin D analogs. Topical calcineurin inhibitors may be used on the face and intertriginous areas. If unable to control, light therapy with either UVB or PUVA may be considered, but requires 2–3 visits/week for months. Traditional systemic therapies including acitretin, cyclosporine, and methotrexate should be considered in patients with moderate to severe psoriasis with >10% body surface involvement or severe functional impairment (hands, feet, arthritis, and genitals). If unresponsive or unable to tolerate these, biologic therapy such as the TNFα inhibitors (infliximab, adalimumab, golimumab, etanercept) or ustekinumab (anti-IL 12/23) should be considered for psoriatic arthritis. Avoid systemic steroids as discontinuation may cause generalized pustular psoriasis
Specific Entities
PITYRIASIS ROSEA
pathophysiology—human herpesvirus-6/7 may be the etiologic agent, although this disorder does not seem to be contagious
clinical features—herald plaque (2–5 cm, round, redder, scaly) followed by many smaller plaques. Resolves spontaneously after 2–5 weeks
treatments—no treatment needed usually. Topical steroid to relieve pruritus
LICHEN PLANUS
pathophysiology—autoimmune disease with lymphocytic infiltration in epidermis
associations—drugs (β-blockers, methyldopa, penicillamine, NSAIDs, ACE inhibitors, carbamazepine, gold, lithium), HCV infection
clinical features ★5 P’s★—Purple, Pruritic, Polygonal, Planar (flat-topped) Papules. May also see fine white lines on the surface (Wickham’s striae). Commonly seen in flexor wrists, forearms, and buccal mucosal (lacy white reticular lesions). Lesions may last for a year
treatments—no treatment needed usually. Topical steroids, antihistamines, and anti-inflammatories to relieve pruritus. Investigate for associated causes
SEBORRHEIC DERMATITIS
pathophysiology—a common skin disorder affecting areas rich in sebaceous glands such as the scalp, face, mid-chest, and intertriginous areas. It is caused by the yeast Malassezia furfur (formerly known as Pityrosporum ovale), M. restricta, and M. globosa, with increased host response leading to dermatitis. It is also known as “dandruff” in adults
clinical features—pink to erythematous plaques with yellow scales or greasy crusts, which may occasionally be pruritic
treatments—gentle emollients, ketoconazole shampoo or cream, and 1–2.5% hydrocortisone cream. Severe scalp involvement in an adult may also be treated with shampoos containing selenium sulfide, zinc pyrithione, and stronger steroid liquids
Related Topic
Psoriatic Arthritis (p. 320)
URTICARIA (HIVES)
pathophysiology—an acute (<6 weeks) or chronic (>6 weeks) type I hypersensitivity reaction. Most cases are idiopathic but triggers may include infections and medications
clinical features—characterized by superficial transient edema with pink highly pruritic papules or plaques with individual lesions having rapid onset and resolution within 24 h. Dermatographism is common where wheals may be induced after stroking the skin
treatments—non-sedating antihistamines during the day and scheduled sedating antihistamines at night. Systemic glucocorticoids may be used when severe, but courses should be tapered over 5–7 days
DERMATOPHYTE (TINEA) INFECTIONS
pathophysiology—Trichophyton, Epidermophyton, Microsporum are fungi that can uniquely dissolve keratin
clinical features—asymptomatic, scaling erythematous patches/plaques that slowly enlarge over scalp (tinea capitis), feet (tinea pedis), hand (tinea manuum), groin (tinea cruris), body (tinea corporis), and nails (onychomycosis). May be associated with pruritus and vesicles
diagnosis—skin and nail lesions may be difficult to distinguish from psoriasis, eczematous conditions, and lichen planus. KOH examination from skin scrapings shows segmented hyphae and spores
treatments—tinea capitis (griseofulvin 20–25 mg/kg/day for 6–8 weeks, terbinafine, itraconazole), tinea pedis or cruris (terbinafine 1% cream daily-BID, clotrimazole/Lotrimin 1% cream BID), onychomycosis (terbinafine 250 mg PO daily × 6–12 weeks, itraconazole 200 mg PO daily × 8–12 weeks. Need to monitor liver enzymes)
TINEA VERSICOLOR
pathophysiology—Malassezia furfur
clinical features—young adult with hypopigmented, light brown, or salmon-colored scaly macules coalescing into patches
diagnosis—KOH examination from skin scrapings show classic “spaghetti and meatballs” pattern representing hyphae and spores
treatments—topical (terbinafine 1% cream daily BID, clotrimazole 1% cream BID, selenium sulfide 2.5% shampoo or lotion), systemic (ketoconazole, fluconazole, itraconazole)
GROIN SKIN LESIONS
—common causes include tinea cruris, candidiasis, erythrasma (Corynebacterium minutissimum), and inverse psoriasis
Acne Vulgaris
NEJM 2005 352:14
Differential Diagnosis of Acneiform Lesions
ACNE VULGARIS
ROSACEA
PERIORAL DERMATITIS
DRUGS
—EGFR inhibitors (erlotinib, gefitinib, cetuximab, panitumumab) and oral corticosteroids (prednisone, dexamethasone) can cause pustular folliculitis
Pathophysiology
PATHOGENESIS
—condition affecting pilosebaceous units, commonly seen during puberty. Pathogenesis involves androgens, follicular keratinization, and the Gram-positive bacteria Proprionibacterium acnes. Lesions may present as non-inflammatory comedones or inflammatory papules. Inflammatory cysts may leave behind hyperpigmentation and sometimes scaring
RISK FACTORS
—drugs (steroids, phenytoin, lithium), androgen excess (PCOS, Cushing’s, congenital adrenal hyperplasia)
Clinical Features
SEVERITY OF ACNE VULGARIS
mild—mainly comedones with few papules/pustules
moderate—moderate papules and pustules (10–40) and comedones (10–40)
moderately severe—numerous papules and pustules (40–100) and many comedones (40–100). May have nodular inflamed lesions (up to 5). Widespread involvement of face, chest and back
severe—nodulocystic acne and acne conglobata with many nodular or pustular lesions
TYPICAL PRESENTATION
—teenager with open comedones (blackheads), closed comedones (white heads), erythematous papules, pustules, cysts and scarring over face, shoulders, upper chest, and back
Investigations
SPECIAL
(not typically performed)
endocrine workup—testosterone, 24-h urinary cortisol
Management
TREAT UNDERLYING CAUSE
first – line agents—topical agents include benzoyl peroxide 2.5–10% daily-BID, sulfur-based washes, topical retinoids (tretinoin 0.025–0.1% qhs, tazarotene qhs), and topical antibiotics (clindamycin daily-BID, erythromycin daily-BID)
moderate cases—oral antibiotic (minocycline 50–100 mg daily-BID, doxycycline 50–100 mg daily-BID, trimethoprim–sulfamethoxazole 160/800 BID, tetracycline 250–500 mg daily-BID, erythromycin 250–500 mg BID–QID) or antiandrogen therapy such as birth control pills may be used in female patients
severe cases—respond well to oral isotretinoin 0.5–1 mg/kg/day, with a cumulative dose of 120 mg/day. Close monitoring with laboratory and clinical follow-up. High risk for teratogenicity
Treatment Issues
RETINOIDS
—inhibit sebum excretion and P. acnes. Reserved for severe nodulocystic acne. Topical retinoids may cause photosensitivity. Retinoids should never be used in pregnant women as highly teratogenic. Fertile women should take oral contraceptive pills 2 months before treatment continuing until 1 month after discontinuing oral retinoids
Specific Entities
ROSACEA
clinical features—middle age adults with central facial telangiectasias, flushing (especially after ingestion of hot liquids, alcohol, spicy foods, and other triggers), and acneiform papulopustules in cheeks, nose, forehead, and chin. No comedones. Maybe associated with rhinophyma (more in men), conjunctivitis, iritis, and keratitis
treatments—oral antibiotics (tetracycline, erythromycin), topical antibiotics (metronidazole 0.75%), sulfur-based products (sodium sulfaceta mid lotion 10%), pulsed dye laser
PERIORAL DERMATITIS
clinical features—young woman with papules and pustules over chin, upper lip, and nasal labial folds
treatments—oral antibiotics (tetracycline, erythromycin)
Exanthematous Lesions
Differential Diagnosis of Exanthematous Lesions
INFECTIONS
viral—HCV, HIV, EBV, parvovirus B19, measles, rubella, roseola
bacterial—toxic shock, Staphylococcal scalded skin syndrome, Streptococcal toxic shock syndrome, scarlet fever, meningococcus, Rocky Mountain spotted fever, typhus
IATROGENIC
—medications (see DRUG ERUPTIONS p. 422)
Clinical Features
TYPICAL PRESENTATION
—widespread erythematous maculopapular lesions that may be accompanied by fever and malaise
Management
TREAT UNDERLYING CAUSE
—discontinue any offending drugs. Usually resolve spontaneously
Related Topic
Fever and Rash (p. 260)
Specific Entities
PARVOVIRUS B19
—slapped cheek rash on face and erythematous eruption on trunk, neck, and extremities. Also called fifth disease or erythema infectiosum. Fever may be present. Parvovirus B19 is also associated with aplastic anemia, polyarthritis, and fetal hydrops
STAPHYLOCOCCAL SCALDED SKIN SYNDROME (SSSS)
pathophysiology—exfoliatins produced by specific strains of staphylococci leading to desquamative disorder with cleavage at the granular layer of the dermis and acute epidermolysis
clinical features—fever, malaise, generalized macular erythematous rash that evolves rapidly into a scarlatiniform (sandpaper-like) rash, followed by an exfoliative phase with perioral exudation and crusting. Large radial fissures “sunburst” around the mouth and are one of the diagnostic features. Nikolsky sign positive. Increased risk in children/infants, renal failure, immunocompromised
diagnosis—culture from a site other than the blisters (blood, conjunctivae, nasopharynx) demonstrating staphylococci
treatments—hospitalization and IV antibiotics for treatment of Staphylococci (nafcillin/oxacillin first line, vancomycin if failing therapy or high prevalence or risk of MRSA)
TOXIC SHOCK SYNDROME
pathophysiology—exotoxin by specific strains of S. aureus or group A Streptococcus (toxic shock syndrome toxin-1 TSST-1) acting as superantigens, activating T cells, leading to cleavage at the granular layer of the dermis
clinical features—young person with fever, malaise, generalized macular, erythematous rash including mucous membranes, palms and soles, evolves into petechiae, vesicles, and bullae. Ulcerations may be seen on mucous membranes. Exclude retained foreign bodies (especially tampons, contraceptive sponges). Hypotension and organ failure may occur
treatments—fluid resuscitation as needed, vancomycin (30 mg/kg/day IV divided BID) or β-lactam plus clindamycin (900 mg IV q8h). If unresponsive to fluids or vasopressors, consider IVIG (400 mg/kg × 1 dose, limited evidence)
SCARLET FEVER
pathophysiology—erythrogenic toxin by specific strains of group A Streptococcus leading to cleavage at the granular layer of the dermis
clinical features—children with fever, sore throat, petechiae, and punctate red macules on hard and soft palate and uvula (Forchheimer spots), circumoral pallor, strawberry tongue, erythematous patches involving ears and chest, extend to trunk and extremities and accentuate in skin folds (Pastia lines). Evolves to sandpaper-like appearance. Desquamation happens 7–10 days after resolution of rash
treatments—antibiotics and fluid resuscitation as needed
Stevens–Johnson Syndrome/Toxic Epidermal Necrolysis
Differential Diagnosis of Vesicles/Bullous Lesions
INFLAMMATORY
—bullous pemphigoid*, pemphigus vulgaris*, porphyria cutanea tarda*, lupus*, dermatitis herpetiformis, erythema multiforme, contact dermatitis
INFECTIONS
bacterial—bullous impetigo*, Staphylococcal scalded skin syndrome, toxic shock syndrome
viral—HSV, VZV, molluscum contagiosum, Coxsackie virus
NEOPLASTIC
—paraneoplastic pemphigus
IATROGENIC
—Stevens–Johnson syndrome*, toxic epidermal necrolysis*
*bullous lesions may be seen with or without vesicles
Pathophysiology
HYPERSENSITIVITY REACTION
—Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) lie on a spectrum of serious, life-threatening illness characterized by extensive epidermal necrosis. By definition, SJS involves less than 10% of the body surface area (BSA) and TEN involves greater than 30% of the BSA. Involvement of 10–30% BSA is an overlap between the two. Drugs are the most common offending agents, but Mycoplasma pneumoniae, viruses, various chemicals and immunizations have also been associated with SJS/TEN
COMMONLY ASSOCIATED DRUGS ★4A’S★
Allopurinol
Antibiotics—sulfamethoxazole, cephalosporins, penicillins, quinolones, macrolides
Anti-inflammatory drugs—NSAIDs, salicylates
Anticonvulsants—carbamazepine, phenytoin, lamotrigine, phenobarbital
Clinical Features
TYPICAL PRESENTATION
—patients usually develop symptoms within 2–3 weeks after drug exposure, more rapidly in previously exposed patients. The prodrome involves a flu-like syndrome with fever, malaise, arthralgias, myalgias, and mucous membrane lesions. This is followed by the development of irregular targetlike lesions often with necrotic centers that coalesce over time. Flaccid blisters form that spread with pressure (Nikolsky sign) resulting in sheet-like loss of epidermis and exposure of the underlying dermis. Ninety percent of patients have mucous membrane involvement and 60% have ocular involvement
NIKOLSKY’S SIGN
—pressing on the edges of an intact blister helps to discriminate between an intraepidermal blistering process (pemphigoid vulgaris, blister extends and breaks easily) and a subepidermal process (TEN, bullous pemphigoid, blister would not advance)
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