Urticaria acute spontaneous L50.8

Urticaria that does not last longer than 6 weeks, which heals spontaneously 2-3 weeks after the first appearance in over 90% of all cases.

Acute urticaria (combined with angioedema in 50% of cases) occurs once in a lifetime in 20-25% of the population (lifetime prevalence).

Polyetiologic genesis!

Infections: An association with acute infections can often be demonstrated and is affirmed in most guidelines. The most frequent associations are with viral infections of the upper respiratory tract. Bacterial infections (sinusitis, urinary tract infections, gastrointestinal infections) can also be causative. The best evidence exists for infection with Helicobacter pylori).

It is not uncommon for a combination effect of infection and medication to occur (especially anti-inflammatory drugs, non-steroidal, in particular aspirin or antibiotics).

Drugs can have a triggering effect in different ways. For example, certain medications (opiates, muscle relaxants, X-ray contrast media, various antibiotics, biologics) can have a triggering effect. antibiotics, biologics) can induce direct histamine liberation. Other drugs (non-steroidal anti-inflammatory drugs) release cysteinyl leukotrienes as part of an analgesic hypersensitivity.

Type I allergies (acute spontaneous allergic urticaria): Type I allergies are detectable as a triggering cause in adults < 1%; in children (often pre-existing atopic eczema) IgE-mediated acute urticaria (mostly food allergies) is detectable in up to 15%. In these cases, other atopic diseases (allergic rhinitis, allergic bronchial asthma, oral allergy syndrome) are also known. The causative food allergies (note: these allergies are usually known to the patients) are triggered by eggs, cow's milk, peanuts, tree nuts, soy, wheat, fish, shellfish (see food allergens below). In Portugal, urticaria (angioedema) caused by fish nematodes(anisakiasis) has been described (Anisakis simplex is a common parasite of fish and anisakiasis is still widespread in Japan, where sushi is often made from freshly caught fish; humans are accidental false hosts).

Intolerance reactions (pseudoallergy) caused by drugs or biogenic amines can occasionally be identified as the cause of acute urticaria.

m:w=1:1; young people are most frequently affected, especially children with atopic dermatitis;

Acutely occurring, raised, sharply defined, palpable, solitary or confluent, itchy, whitish to red wheals. The size of the efflorescences can be very variable, from pinhead-sized to extensive. Mostly urticae develop within a few minutes after histamine release. Occasionally the orange peel phenomenon can be triggered. The disease heals within a maximum of 6 weeks, usually within 1-2 weeks.

A special clinical form of acute urticaria is the ( histamine-induced) angioedema, which is accompanied by acute swelling of the face, especially the lips and eyelids.

Eliminate or avoid a triggering agent (infection, medication, food allergens) as far as possible. Often the causes cannot be determined. The therapy should then be directed towards symptomatic acute therapy.

Cooling moist compresses on the face (0.9% NaCl solution), anti-itching lotion with the addition of e.g. Polidocanol 2-5% as a finished product (e.g. Optiderm Lotion/Creme), as a formulation (e.g. Polidocanol-Creme 2-5% or R200) or 1% menthol solution.

Alternatively, glucocorticoid-containing creams/emulsions like 0.5-2% hydrocortisone cream or emulsions like R123, R120.

Advice: The frequently used antihistamine-containing gels (e.g. Fenistil, Tavegil, Soventol) show moderate success.

• Localized form: For itching oral, non-sedative antihistamines such as desloratadine (Aerius) once/day 10 mg p.o. or levocetirizine (Xusal) once/day 5 mg p.o.
• Generalized form without mucosal involvement: In acute attacks, antihistamines i.v. such as dimetinden (e.g. Fenistil) 1-2 times/day 1 amp. i.v. or clemastine (e.g. Tavegil) 2-4 mg i.v. Later switch to oral non-sedating antihistamine. Glucocorticoids in medium dosages such as prednisolone (e.g. Solu Decortin H) initially 50-100 mg i.v., then gradual dose reduction depending on the clinic. Later switch to an oral preparation such as methylprednisolone (e.g. Urbason) or prednisolone.
• Generalized form with mucosal involvement and angioedema: volume substitution, glucocorticoids in high doses i.v. like prednisolone (e.g. Solu Decortin H) 250-500 mg, possibly even higher. After clinical findings, repeated administration may be necessary. Gradual dose reduction according to clinical findings 250-150-100-75-50-25 mg and switch to oral preparation such as methylprednisolone (e.g. Urbason).
  Antihistamines initial e.g. Dimetinden (e.g. Fenistil) 4 mg i.v. (conversion to oral medication up to 6 mg/day, reduction according to clinic) or Clemastine (e.g. Tavegil) 2-4 mg.
• For laryngeal glottis oedema: Additional adrenalin (suprarenin 1:1000) 0.3-0.5 ml s.c., repeated administration also possible. In highly acute cases: after diluting 1 ml of the commercially available epinephrine solution (1:1000) to 10 ml or using a pre-filled epinephrine syringe (1:10,000), 0.5-1.0 ml (= 0.05-0.1 mg epinephrine) is first injected slowly i.v. (0.1 mg/min.) under pulse and blood pressure control.

• Cave! A maximum dose of 1 mg adrenaline should not be exceeded as a rule.

• Notice!

  Risk of arrhythmias up to ventricular fibrillation and myocardial ischemia! Oxygen delivery 4-6 liters per minute. Intubation if necessary. Ultima ratio are coniotomy or tracheotomy.
• Especially in cases of respiratory distress and concomitant obstructive respiratory disease, injection of terbutaline sulphate (e.g. Bricanyl) 0.5-2.0 mg/day i.v. or fenoterol (e.g. Berotec dosage aerosol) once 1 stroke.
• Generalized form with angioedema and anaphylactic shock: Stage-specific shock therapy.

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