Dermatitis L30.9; L30.8

In the broader sense of general pathology: inflammation of the skin.

In the strict sense: Acute to chronic, inflammatory, non-infectious intolerance reaction of the epidermis and corium, caused by a multitude of exogenous noxae and endogenous reaction factors.

In Anglo-American usage, eczema is increasingly replaced by dermatitis.

A distinction is made between acute dermatitis and chronic dermatitis.

The classification is often based on a wide variety of criteria, e.g. appearance, localisation, age or aetiology.

• Initial redness: stage erythematosus.
• Formation of small nodules: stage papulosum.
• Formation of vesicles: stage vesiculosum.
• Bursting of vesicles: stage madidans.
• Crusting of the weeping surfaces: stage crustosum.
• Desquamation: stage squamosum.
• Residual reddening: resterythema.
• Healing: Restitutio ad integrum.

According to a scheme varied by Ackerman, 8 different fabric patterns can be defined. These differ in

• their topographic pattern (superficial/deep)
• their relationship to the surface epithelium and skin appendages
• their relationship to the supplying structures (perivascular; perineural)
• its infiltrate composition (granulocytic/lympho-plasmocytic/epitheloid).

Depending on the location, arrangement and composition of the infiltrate in the dermis and epidermis, a distinction is made between:

1. Superficial, perivascular/interstitial dermatitis
2. Superficial and deep perivascular/interstitial dermatitis
3. Nodular dermatitis
4. Diffuse dermatitis
5. Subepidermal, vesicular dermatitis
6. Folliculitis and perifolliculitis
7. Fibrosing dermatitis
8. Vasculitis (small and large vessel).

Since the epithelial inflammatory response is often of groundbreaking importance for the histological diagnosis, the reaction patterns of the epithelium are additionally classified in the histological diagnosis. Basically the following 3 reaction types (R) are distinguished, which are also transferable to the clinical-morphological area:

• R1 spongiotic-vesicular (eczematous dermatitis)
• R2 psoriasiform (psoriasiform dermatitis)
• R3 lichenoid (lichenoid dermatitis).

The spongiotic vesicular reaction is distinguished according to the type of vesiculation and its localization:

• Vesiculation type (V):
  • V1 spongiotic
  • V2 Ballooned
  • V3 acantholytic.
• Localization (L):
  • L1 suprabasal
  • L2 intraspinal
  • L3 subcorneal.

Switching off the triggering noxae, phase-specific therapy, according to the prevailing clinical findings. Particularly in the case of chronic dermatitis, test ointment tolerance as quickly as possible (epicutaneous, lapping test, quadrant test). Selection of suitable or as far as possible indifferent bases (e.g. aqueous solutions, vaselinum alb.). Especially no wool waxes and wool wax alcohols! If glucocorticoid sensitization is suspected, if necessary use 0.1% mometasone (e.g. Ecural ointment, fat cream, solution), as no cross allergies have been described so far.

• Acute dermatitis

  :Remember!

  Basic principle: the more acute and weeping the dermatitis, the more watery the base!
  Acute vesicular to bullous stage (oozing): Short-term glucocorticoids of medium to strong potency such as 0.1% triamcinolone (e.g. triamgals, R259 ), 0.25% prednicarbate (e.g.Dermatop cream/ointment), 0.1% mometasone (e.g. Ecural fat cream, ointment) or 0.05% clobetasol (e.g. R054, Dermoxin cream/ointment) depending on the clinic and localisation. No isolated application of fatty bases, but better solutions or hydrophilic creams like Ungt. emulsif. aq. (e.g. R259, R054, Dermatop cream, Ecural Lsg.). If a greasy base is required, it should be applied in combination with moist compresses. Moist compresses are also indicated in combination with hydrophilic creams. Envelopes with e.g. Ringer's solution, in case of superinfection with antiseptic additives like quinolinol (e.g. Chinosol 1:1000), octenidine, R042 or potassium permanganate (light pink).
  In the vesicular stage also fat-moist with glucocorticoid like 1% hydrocortisone in lipophilic base like Vaselinum alb. (hydrocortisone ointment 1%), verba)d moistened above it (e.g. Ringer's solution) or possibly cotton gloves.

  Cave!

  Restrained use of glucocorticoids on sensitive skin areas such as face, neck, intertrigines (submammary, groin region, ano-genital region)!
  Crusty or squamous stage: Hydrophilic creams with the highest possible lipid content to regenerate the skin (e.g. base cream (DAC), Linola cream, Ash base cream, Excipial cream, Eucerin, Dermatop base cream). If necessary also with wound healing additives like dexpanthenol (e.g. R064, Bepanthen ointment).
  After treatment: Nourishing and moisturizing topicals in a compatible base (e.g. Linola Fett N, Asche Base Ointment, Excipial Almond Oil Ointment) possibly with 2-10% urea (e.g. R102, R107, Basodexan Cream, Excipial U Lipolotio, Eucerin 10% Urea Lotio).
• Chronic Dermatitis

  :Remember!

  Basic principle: the more chronic the dermatitis, the more greasy the base!
  Short-term glucocorticoids of medium to high potency see above in a greasing base (e.g. Ecural fat cream, Dermatop ointment). Afterwards antiphlogistic topicals like Pix lithanthracis. On a trial basis Pix lithanthracis 2% in zinc oil (coal tar-zinc oil 2-5%) or coal distillate containing or shale oil sulphonate containing topicals (e.g. ichthosin, ichthoderm, tar-linola fat). Soaps and detergents are to be omitted, instead oil-containing baths (e.g. Balneum Hermal, Balneum Hermal Plus, Balmandol, Linola Fat-Oil Bath), possibly also tar-containing oil baths such as Ichtho Bath. In case of chronic hyperkeratotic and strongly scaling plaque-like dermatitis lesions (see also eczema, hyperkeratotic-rhagadiform eczema of the hands and feet), strongly potent glucocorticoids possibly under occlusion like clobetasol propionate (dermoxin).

  Cave!

  Glucocorticoids in childhood! No treatment under occlusion!
  From the subacute dermatitis stage on, the combination of external therapy with UV therapy is recommended. Cave! Phototoxic and photoallergic dermatitis! A high-dose UVA1 treatment has proven to be effective in dermatitis therapy as well as the combination of brine baths with subsequent UVB irradiation. In case of therapy failure, PUVA bath therapy localized to the lesion is recommended.

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