Contact dermatitis (overview) L25.9

Mostly localized, more rarely (if preceded by sensbilization) disseminated disseminating dermatitis (syn. eczema) caused by:

• exogenous
• acute toxic
• cumulative (chronic) toxic
• or by sensitizing contact toxins.

Under clinical or etiopathogenetic aspects, different classifications can be made.

• They can be distinguished according to temporal aspects:
  • Acute contact dermatitis
  • Subacute contact dermatitis
  • Chronic contact dermatitis.
• Taking into account the aetiology (allergic, irritant) the following contact dermatitis can be distinguished:
  • Allergic:
    • Contact dermatitis, allergic (type IV allergy, contact noxae: protein-bound haptens)
    • Protein contact dermatitis (IgE-mediated contact eczema; contact noxae: protein)
    • Contact dermatitis, haematogenous scattering
    • Dermatitis, photoallergic (type IV allergy; contact noxae: protein bound hapten+UV rays or even visible light)
  • Irritant:
    • Contact dermatitis, toxic (acute or chronic; contact noxious agents: wet work, detergents; chemicals)
    • Phototoxic contact dermatitis (prototype is the "simple" sunburn; also triggered by the combination of contact noxe = light sensitizing agent + UV rays; prototype = meadow grass dermatitis).
• From a topographical point of view the following contact dermatitis can be distinguished:
  • Hand (and foot) dermatitis
  • Fingertip dermatitis
  • lip dermatitis
  • Eyelid dermatitis
  • Dermatitis of the auditory canal (Otitis externa)
  • Genital dermatitis (scrotal or vulvar dermatitis)
  • Diaper dermatitis
  • Analdermatitis
  • Stoma dermatitis
• In diagnoses of contact dermatitis, the duration, aetiology and topography are often taken into account, resulting in terms such as:
  • Cumulatively toxic hand dermatitis
  • Chronic, contact allergic eyelid dermatitis
  • Chronic, toxic genital dermatitis
  • Chronic, contact allergic lower leg dermatitis.

The clinical features of the "eczema reaction" depend on the stage of the acute reaction, but also on the noxious agent involved and the type of contact, pathomechanism, localisation and other factors. The clinical features are clearest in toxic contact dermatitis; this dermatitis variant is therefore considered a prime example:

• The acute stage of the dermatitis is characterized in the mildest case by erythema at the site of the noxious agent, traces of abrasions are possible; if the reaction is more severe, spongy vesicles appear. If the reaction is more severe, spongiotic vesicles appear. If the reaction is more intense, vesicles filled with clear fluid and usually itching severely determine the clinical picture. The vesicles are usually only short-lived; bursting causes the lesion to ooze violently; drying of the exudate causes crust formation, and short-term exposure to the noxious desquamation with restitutio ad integrum. Acute contact dermatitis is therefore a uniform, synchronous sequence of pathological events.
• The chronic stage occurs when the noxious agent continues to be effective and spontaneous healing of the eczema does not occur or the dermatitis persists independently of the noxious agent: The uniformity of the eczema plaque is dissolved by focal emphasis on more exudative or more scaly changes, the formerly sharp border becomes blurred; the skin becomes more voluminous due to increased infiltration of inflammatory cells, the skin folds thicker, the inevitable consequence is a coarsening of the skin texture. Finally the inflammatory phenomena recede into the background and hyperkeratoses, rhagades and lichenification determine the picture.

The morph of dermatitis differs depending on the body region as well as on the type and aggressiveness of the triggering agent and the distribution pattern provides important clues as to the type of triggering.

• Acute irritant contact dermatitis is characterized by rapid onset (within hours) after exposure, which is usually easy to determine, by rapid progression and usually rapid regression, by its monomorphic and often quite intense appearance (up to skin necrosis), more burning and painful than itchy subjective symptoms, the sharp limitation to the contact area and the absence of scattering phenomena.
• Chronic irritant contact dermatitis occurs only after exposure, sometimes lasting up to years, and is characterized by a dry, hyperkeratotic-scaly, cracky-rhagadiform and only slightly exudative character. It proceeds slowly and also heals slowly, is only largely restricted to the contact area and likewise does not tend to scatter. The first symptom is usually an unpleasant dryness of the skin followed by erythema and scaling. Typical predilection sites of the initial symptoms are the back of the hand and the spaces between the fingers. In contrast to the irritative ones, the allergic contact reactions tend to be more scattered. These scattering phenomena can be caused by generalised allergen contact, by haematogenic spread of an allergen or by dissemination of the immune response.

Individually predisposing factors are of great importance especially in chronic degenerative dermatitis, such as underlying atopy or desiccation of the skin mostly caused by age or poor care. Combined clinical pictures are therefore frequent, graft allergies (development of an allergic contact eczema in pre-existing chronic degenerative eczema) not uncommon. These mixed patterns are often not clearly distinguishable from each other in terms of differential diagnosis and clinical practice. Infection by bacterial germs (especially in the case of weeping dermatitis), dermatophytes (hands and feet) or yeast fungi (body folds in infants and diabetics), more rarely also by viruses, complicate the diagnosis, course and therapy of all forms of dermatitis. Pustules on the bottom of a dermatitis can, however, also occur after occlusive ointment treatment and not only due to superinfection. The different localisations not only provide indications of possible triggers but also, to a limited extent, of the pathogenetic mechanisms: for example, photoallergic dermatitis is limited to light-exposed areas and omits regions of the face shaded by the chin, ears, etc. and those parts of the body covered by hair or clothing. Dermatitis of the freely carried body parts can also be caused by aerogenic allergens (such as plant allergens) as well as volatile substances of professional life (e.g. epoxy resins).

Dilated vessels in the papillary str. and in the upper reticular str. with varying degrees of oedema and perivascular infiltrates of lymphocytes and isolated neutrophil and eosinophilic granulocytes. Exocytosis and spongiosis and consecutively by tearing of the intercellular connections blister and bubble formation.

Remember! For irritant dermatitis the following specifications are used among others: toxic, degenerative, sub-toxic, cumulative-toxic, etc.

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4. Smith HR et al (2002) Irritant dermatitis, irritancy and its role in allergic contact dermatitis. Clin Exp Dermatol 27: 138-146
5. Tavadia S (2003) Allergic contact dermatitis in venous leg ulcer patients. Contact Dermatitis 48: 261-265
6. Wildemore JK et al (2003) Evaluation of the histologic characteristics of patch test confirmed allergic contact dermatitis. J Am Acad Dermatol 49: 243-248