Vesicles/Bullae/Pustules
Differential Overview
Vesicles
❑ Herpes simplex
❑ Contact dermatitis
❑ Varicella/zoster
❑ Dyshidrotic eczema
❑ Scabies
❑ Erythema multiforme
❑ Coxsackievirus
❑ Dermatitis herpetiformis
Bullae
❑ Friction blister
❑ Bullous impetigo
❑ Diabetic bullae
❑ Fixed drug eruption
❑ Frostbite
❑ Porphyria cutanea tarda
❑ Staphylococcal scalded skin syndrome
❑ Toxic epidermal necrolysis
❑ Coma bullae
❑ Pseudoporphyria
❑ Pemphigus vulgaris
❑ Bullous pemphigoid
❑ Variegate porphyria
Pustules
❑ Acne vulgaris
❑ Rosacea
❑ Folliculitis
❑ Furuncle
❑ Candida
❑ Gonococcemia
❑ Pustular psoriasis
❑ Hiradenitis suppurativa
❑ Ecthyma gangrenosum
Diagnostic Approach
Vesicles are less than 5 mm in diameter, and bullae are larger. If bullae, petechiae, purpura, or necrosis are present, look for an “allergen” such as HSV, strep, deep fungal infection, collagen disease (especially lupus), or occult neoplasm.
Erythema multiforme can be differentiated from a drug reaction by a dusky violet color and petechiae at the center of the lesion. A target or iris lesion is also characteristic of erythema multiforme.
Staphylococcal scalded skin syndrome can be differentiated from toxic epidermal necrolysis by superficial blisters and absence of oral lesions.
Multidermatomal or disseminated zoster in a young adult should suggest HIV infection.
Clinical Findings
Herpes simplex Lesions appear as grouped vesicles on an erythematous base. Systemic illness, characterized by fever, malaise, headache, and myalgias, is common in primary infection. Common sites of occurrence include the oral mucosa, vermilion border of the lip, the external genitalia, and the finger by inoculation (herpetic whitlow). Tender regional adenopathy is also found. Persistent ulcerative HSV lesions are common with HIV.
Contact dermatitis The hallmark is a circumscribed pattern that reflects the mode of contact. A linear appearance is seen with contact with a plant such as poison ivy.
Varicella/zoster The initial lesions are vesicles on an erythematous base; these coalesce. Varicella can be recognized by lesions present simultaneously in several stages (vesicles, bullae, crusting). An outbreak of zoster is preceded by a dysesthesia, and it occurs in a unilateral dermatomal distribution.
Dyshidrotic eczema Deep, very pruritic microvesicles appear on the sides of the fingers.
Scabies Burrows appear as small linear vesicles in the axilla, flexor wrists, interdigital fingers, waist, and genitalia. The skin is excoriated.
Erythema multiforme Primary lesions are pink-red macules and edematous papules, which develop a dusky violet color or occur as petechiae, which develop central vesicles. Target/iris lesions are also characteristic although not universally present. Lesions occur preferentially on the hands, palms, soles, extensor forearms, and mucous membranes. Hemorrhagic crusts of the lips are often seen. Common causes include drugs, HSV (7 to 12 days after the primary lesion), M. pneumoniae, EBV, coxsackievirus, and influenza virus.
Coxsackievirus In hand, foot, and mouth disease, oval gray vesicles with a red halo appear on the sides of the fingers, ankles, and tongue.
Dermatitis herpetiformis There is intense pruritus with a distinctive burning or stinging component. The primary lesion is a papule, papulovesicle, or urticarial plaque, symmetrically distributed over the extensor surfaces. Gluten sensitivity, although usually present, is otherwise subclinical.
Friction blister They are easily identifiable as painful bullae at the site of friction/trauma, such as on the heel during a long hike.
Bullous impetigo It appears as honey-colored crusts and purulent blisters on a weeping red base.
Diabetic bullae Tense bullae filled with clear fluid may arise on normal skin. These lesions appear on the distal extremities, and may be several centimeters in diameter.
Fixed drug eruption Blisters with an erythematous base recur stereotypically in the same location with repeated drug exposure, commonly on the orogenital mucosa.
Frostbite Hemorrhagic bullae are characteristic, as is the history.
Porphyria cutanea tarda In sun-exposed areas, such as the hands and face, minor trauma may lead to erosions and tense vesicles. These heal with scarring and often form milia (2 to 3 mm white or yellow papules). Malar hypertrichosis, and hyperpigmented, sclerotic plaques also occur. Precipitating agents include alcohol, estrogen, iron, and chlorinated hydrocarbons.
Staphylococcal scalded skin syndrome It begins as redness and tenderness in the face, neck, trunk, and intertrigonal zones, and is followed by short-lived flaccid bullae. Crusting then develops, especially around the mouth.
Toxic epidermal necrolysis Bullae arise on widespread areas of erythema and then slough. Friction applied to normal skin causes separation and bunching of the epidermis (Nikolsky sign). Drugs are the most common cause, including phenytoin, penicillin, sulfonamides, barbiturates, allopurinol, NSAIDs, and phenolphthalein.
Coma bullae These occur classically with barbiturate coma, from the patient lying motionless.
Pseudoporphyria Clinically similar to porphyria cutanea tarda, it is caused by photosensitivity induced by furosemide, tetracycline, nalidixic acid, dapsone, naproxen, or pyridoxine.
Pemphigus vulgaris Lesions consist of flaccid blisters that rupture easily, leaving denuded areas that crust and enlarge readily. The Nikolsky sign is also present. In more than half, lesions begin in the mouth, but also commonly occur on the scalp, face, neck, axilla, and trunk.
Bullous pemphigoid Tense, thick-walled blisters develop on normal-appearing or erythematous skin. They are distributed over the abdomen, groin, flexor surfaces, and oral mucosa. As bullae rupture, they leave flaccid erosions without crust. Hundreds may appear within days.
Variegate porphyria It has the skin signs of porphyria cutanea tarda and the systemic findings of acute intermittent porphyria.
Acne vulgaris Red papules and pustules on the face and upper back appear during adolescence.
Rosacea Acneform lesions occur in adulthood. Look also for telangiectasias and sebaceous activity in the central face. Rosacea worsens with alcohol, spicy food, heat, and stress.
Folliculitis Scattered or clustered, follicular-based (central hair) red pustules appear. In staphylococcal infections, look for honey-yellow crusts. If the onset is after bathing in a spa, pseudomonas is the likely organism.
Furuncle Deep, red lesions with pustular centers are found mostly on the face, neck, or buttocks.
Candida A bright red confluent plaque with satellite pustules develops in intertriginous areas.
Gonococcemia Hemorrhagic pustules appear on the extremities; these are associated with tenosynovitis, fever, and arthritis.
Pustular psoriasis This is a generalized process with a mixture of red scaling plaques and flat pustules.
Hiradenitis suppurativa Occurs in apocrine sweat glands in the axilla and inguinal region. Early in the condition lesions are pustules, but later there may be extensive scar formation. Comedones are also present.
Ecthyma gangrenosum A burning, painful lesion with central crusting develops in gram-negative (e.g., pseudomonas) sepsis.
Book Source Details
- Book Title: Field Guide to Bedside Diagnosis
- Author(s): David S. Smith
- Year of Publication: 2007
- Copyright Details: Field Guide to Bedside Diagnosis, Copyright © 2007 Lippincott Williams & Wilkins.
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Copyright Details: Field Guide to Bedside Diagnosis, Copyright © 2008 Williams & Wilkins.
More About Causes of Blisters
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More About This Book:
Title: Field Guide to Bedside Diagnosis
Authors: David S. Smith
Publisher: Lippincott Williams & Wilkins
Copyright: 2007
ISBN: 0-78178-165-5
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