Anaphylaxis T78.2

Anaphylaxis is the maximum variant of the allergic immediate reaction, which can affect the entire organism as an acute onset and potentially fatal mast cell-dependent systemic reaction. According to Sampson, anaphylaxis (anaphylactic reaction) is characterized by the onset of symptoms in 2 or >2 organ systems within minutes to hours after contact with a known allergic trigger. It is of short duration.

Rarely, an anaphylactic reaction has been triggered by circulating immune complexes. Anaphylaxis can also be triggered by a non-allergic mechanism (direct release of mediators) (no preceding sensitization). These reactions are called "pseudoallergic anaphylaxis or non-immunological anaphylaxis".

According to Ring and Messmer, the following clinical classification of the severity of anaphylaxis applies:

A distinction is made:

• Classic anaphylactic reaction (type I reaction; IgE-mediated; see below allergy)
• Anaphylaxis, wheat-dependent, exertion-induced
• IgE-independent intolerance reaction (anaphylactoid or pseudoallergic reaction).

All clinical reactions follow an identical pattern.

Prevalence figures are usually inaccurate and range from 1.5-15% in the general population. About 3% of the population is affected by bee or wasp venom anaphylaxis. Besides insect venoms, the most common triggers of anaphylaxis are food, drugs, natural latex, physical exertion and physical factors (cold/heat). The spectrum of triggers is different in children and adults:

• in children are food
  • children < 6 years: chicken protein and milk protein
  • Children > 6 years: tree nuts, peanuts
• in adults, insect venoms and drugs are the most common triggers of anaphylaxis.

There are also different age-related triggers for drug-induced anaphylaxis:

• Children: beta-lactam antibiotics
• Adults: NSAID

The central initial mechanism of classical, IgE-mediated anaphylaxis is the activation of mast cells and basophilic granulocytes. In this process numerous mediators such as histamine, prostaglandins, leukotrienes, tryptases are released abruptly (on/off reaction). This results in vasodilatation and increased permeability, contractions of smooth muscles (bronchi, gastrointestinal tract, coronary arteries), vagus activation as well as activation of the kinin-Kallikrein signaling pathway, the complement system and the coagulation system.

Cofactors of anaphylaxis are factors that can lower the threshold for an anaphylactic response. These include non-steroidal anti-inflammatory drugs, ACE inhibitors, beta-blockers (see also intolerance reaction), alcohol, infections, exertion.

In addition to IgE, immune complexes can also trigger anaphylaxis.

In intolerance reactions, chemical, physical and osmotic stimuli lead to the release of mediator substances from mast cells and basophilic granulocytes. The initiating mechanisms are largely unexplained.

It is not uncommon for anaphylaxis to occur only in the presence of one or more co-factors (e.g. food + acetylsalicylic acid + alcohol; food + acetylsalicylic acid + effort; food + acetylsalicylic acid + systemic mastocytosis). These constellations are particularly difficult to diagnose, as they only become clinically apparent in the combinations in question.

S.U.S. shock, anaphylactic.

S.U.S. shock, anaphylactic.

Anaphylaxis and atopy are not synonymous terms. Atopy denotes a property, anaphylaxis a reaction.

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