Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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Bubbles; Bulla; bullae

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A non-solid skin ridge filled with tissue fluid (clear, serous, hemorrhagic).

A bladder is based on a single- or multi-chambered, 1.0 to > 5.0 cm large (rarely larger), intra- or subepidermal cavity consisting of the bladder floor, ceiling and contents. Bubbles < 1.0 cm are called vesicles or vesiculae.

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From a pathogenetic point of view, blisters can be distinguished by the location of the bladder:
  • Intraepidermal blistering:
    • acantholytic
    • spongy
    • cytolytic
  • Junctional bubble formation
  • Dermolytic blistering (below the basal lamina)
  • Dermal blistering due to focal oedema.
The wall of intraepidermal vesicles is thinner, therefore it tears more easily and is often covered with a crust when the contents dry up. The wall of subepidermal vesicles is thicker and therefore more resistant and due to its deep seat more often hemorrhagic.

General information
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  • The possibility of genetic blistering (familial occurrence, first clinical symptoms) must be taken into account in the anamnesis or possibly excluded.
  • During the clinical examination, localisation (face, trunk, mechanically exposed areas, mucous membranes), distribution pattern (solitary, disseminated, exanthematic), arrangement (grouped, anular, herpetiform), size, shape, wall structure and the content of the bladder itself (acantholytic cells, leucocytes) as well as the condition of the surrounding skin (inflammatory or normal) are to be evaluated.
  • Of differential diagnostic importance are accompanying symptoms such as itching (light and burning in dermatitis herpetiformis Duhring) and pain (various epidermolyses).

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  • Bubble formation can be autoimmunological or non-autoimmunological. In autoimmunological blistering, high-affinity antibodies are formed which are directed against a single or a few antigens specific for the skin (and the mucous membranes close to the skin). The clinical-morphological consequences of blistering are largely identical for all diseases, as they are characterized by their sequelae, e.g. erosions, crusts, secondary infections, scars.
  • In the case of non-immunological blistering, different scenarios for blistering are possible:
    • Genetically caused structural weakness of e.g. keratins or anchor fibrils (e.g. epidermolysis)
    • Blistering due to tissue loss (cytolytic blistering, e.g. zoster, herpes simplex, burns)
    • Non-immunological inflammatory processes of various causes with consecutive "suppressive" oedematous blistering in the epidermis (spongiotic blistering) or dermis (dermal oedema). Examples of this are bullous eczema reactions, bullous urticaria or bullous mastocytosis.

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  1. Altmeyer P (2007) Dermatological differential diagnosis. The way to clinical diagnosis. Springer Medicine Publishing House, Heidelberg
  2. Nast A, Griffiths CE, Hay R, Sterry W, Bolognia JL. The 2016 International League of Dermatological Societies' revised glossary for the description of cutaneous lesions. Br J Dermatol. 174:1351-1358.
  3. Ochsendorf F et al (2017) Examination procedure and theory of efflorescence. Dermatologist 68: 229-242


Last updated on: 29.10.2020