Anaphylaxis
| Classification according to ICD-10 | |
|---|---|
| T78.0 | Anaphylactic shock from food intolerance |
| T78.2 | Anaphylactic shock, unspecified |
| T80.5 | Serum anaphylactic shock |
| T88.6 | Anaphylactic shock as an undesirable side effect of an indicated medicinal product or an indicated drug when properly administered |
| ICD-10 online (WHO version 2019) | |
The anaphylaxis (formed incorrectly from ancient Greek ἀνά ana "on (-wärts) again", and φύλαξις phylaxis "guarding, safekeeping") is an acute , allergic response of the immune system of humans and animals to repeated supply of exogenous proteins and affects the whole organism.
The picture of anaphylactic reactions ranges from mild skin reactions to disturbances of organ functions to anaphylactic shock ( circulatory shock with possible organ failure to fatal circulatory failure ).
Pathogenesis and physiology
Anaphylaxis is an overreaction of the adaptive immune system . This results in excessive release of mediator substances ( histamine , leukotrienes , etc.) by mast cells and basophilic granulocytes , which can be caused by the mediating effect of special antibodies ( immunoglobulin E ).
They require awareness . After the first antigen contact of plasma cells, an antibody of the IgE type is secreted (released), which attaches to basophilic granulocytes and mast cells with the Fc content. The free Fab part of the IgE molecule thus points into the extracellular space .
The reaction of antigens with these cellular IgE antibodies is fundamental , corresponding to a type 1 reaction according to Gell and Coombs . The antigen ( molar mass 10,000 to 70,000 u ) usually has two epitopes , so that bridges between IgE antibody molecules occur.
After stimulation by the antigen, the basophilic granulocytes and the mast cells release mediators ( histamine , prostaglandins , leukotrienes , platelet-activating factor (PAF) and others) and cytokines .
The mediators lead to the clinical picture of anaphylaxis (see below). The secretion of the cytokines in turn leads to the attraction of neutrophils and thrombocytes , which in turn release further mediators that are important in the inflammatory process.
The effects of the released mediators are
- increased vascular permeability (permeability of the vascular walls)
- Vasodilation (widening of vessels) and
- Bronchospasm (constriction of the bronchi).
causes
A distinction is made between the classic anaphylactic reaction, which is an IgE-mediated allergic event, and the IgE-independent anaphylactoid reaction.
Both events follow the same clinical picture. In anaphylactoid reactions, however, it is not contact with IgE antibodies, but chemical, physical and osmotic stimuli that lead to the release of mediator substances from mast cells and basophilic granulocytes.
Idiopathic anaphylaxis
So-called idiopathic anaphylaxis, in which the specific trigger cannot be determined, can u. a. caused by underlying and undiagnosed mast cell diseases (such as mast cell activation syndrome / MCAS or systemic mastocytosis ), as these lead to an excessive release of mast cell mediators.
clinic
The extent of the allergic reaction can vary greatly from person to person. An anaphylactic reaction has two phases:
- Initial phase and
- systemic response.
Initial phase
Within minutes to hours:
Systemic response
The following develop
- generalized skin symptoms ( itching , flushing of the face , general inflammatory skin reddening, so-called erythema , hives )
- Airway obstruction ( obstruction ) by edema in the throat ( pharynx -) and throat area ( larynx ) and bronchospasm and pulmonary edema
- Gastrointestinal symptoms with colic, vomiting, diarrhea ( diarrhea )
- Haemodynamic changes due to fluid displacement and vasodilation ( vasodilation ), which can lead to shock .
Anaphylactic shock
An anaphylactic shock is a life-threatening anaphylaxis. He can z. B. by insect venom, food, infusions, immune serum or blood serum administration, animal allergens or (in the case of a drug allergy) drugs. The widening of the blood vessels leads to a sharp drop in blood pressure , and fluid leaks from the vessels into the surrounding tissue. Due to the drop in blood pressure, there is a reduced blood flow to vital organs.
The faster the symptoms appear during the injection of a drug, the more life-threatening the condition. In the worst case, the first symptoms appear ten seconds after the injection has started. These are very unspecific - e.g. B. nausea, circulatory problems, nausea or vomiting, dry mouth, burning tongue, visual disturbances, acute shortness of breath, concentration disorders.
Skin reactions, itching, wheals or the development of eyelid edema are also possible, but often completely absent because of the rapid development.
As the process progresses, the typical symptoms of shock appear; H. the pulse becomes flat and rapid and unconsciousness and subsequent death can occur.
Systematics and therapy
Anaphylactic reactions are classified into four degrees of severity:
| Severity | Symptoms | therapy | |
|---|---|---|---|
| 0 | locally limited skin reaction | ||
| 1 | slight general reaction | disseminated skin reaction (flush, urticaria), mucosal reactions, general reaction (restlessness, headache) | H 1 and H 2 antagonists , intravenous prednisolone |
| 2 | pronounced general reaction | Circulatory dysregulation, shortness of breath, urgency of stool and urination | Adrenaline im, crystalloid volume therapy, iv prednisolone, H 1 and H 2 antagonists, inhale O 2 and β 2 mimetics in the event of a pulmonary reaction |
| 3 | threatening general reaction | Shock , bronchospasm , dyspnoea , decreased consciousness | Adrenaline im, crystalloid volume therapy, pulmonary: β 2 -mimetics / inhale adrenaline , intravenous prednisolone, theophylline (not recommended for shock because of its antihypertensive effect), possibly also cautiously iv adrenaline |
| 4th | vital organ failure | Respiratory arrest, cardiac arrest | Resuscitation rules |
Shock therapy:
At the first signs of shock (sweating, nausea, cyanosis ), the injection is interrupted, as far as possible, or allergen exposure is ended. If a doctor is not yet present, an emergency call should be made. The patient is shocked by lifting the legs and, if available, oxygen is given through a mask. Unconscious are in the recovery position brought in a cardiac arrest is the resuscitation begun.
If the anaphylactic shock is triggered outside of medical supervision (e.g. by a wasp sting or food allergy), autoinjectors containing adrenaline can be used to alleviate the acute symptoms.
The doctor creates a venous access and begins volume therapy with crystalline electrolyte solutions ( Ringer's solution , saline solution ). In the event of unconsciousness and / or breathing disorders, intubation and artificial ventilation must be considered. Drug therapy consists of intramuscular or intravenous administration of adrenaline , glucocorticoids and antihistamines (combined administration of H1 ( clemastine , dimetinden ) and H2 antagonists ( cimetidine or ranitidine )).
Emergency self-treatment
People with a known risk who could suffer anaphylaxis on contact with a certain allergen, e.g. insect venom, have the option of carrying an emergency kit with them so that they can give themselves a life-saving adrenaline injection before the doctor or paramedic even arrives can. Even then, an emergency doctor has to be called in. The emergency kits also contain a fast-acting antihistamine and cortisone.
history
In 1902 Paul Portier and Charles Richet described the following phenomenon: They injected dogs with an extract from the venomous sting of the velvet anemonefish . The surviving test animals received the poison again two weeks later. The hoped-for immunity or protection against the toxin (phylaxis) did not materialize. Instead, the dogs went into shock. The blood pressure fell, the blood could no longer clot, and changes in the intestinal wall were pathological. This condition has been called anaphylaxis or anaphylactic shock . The term “anaphylaxis” coined by Richet should be an expression for the opposite of “phylaxis”, Greek for “protection”, and should - when using the α-privatum - correctly be called “aphylaxis”. In 1909 Artur Biedl and Rudolf Kraus put forward the theory that the body's own substances are responsible for the reaction. A year later isolated and identified Henry Dale and George Barger of ergot , the histamine .
literature
- S2k guideline for anaphylaxis, acute therapy and management of the German Society for Allergology and Clinical Immunology (DGAKI). In: AWMF online (as of December 31, 2013)
- Werner E. Gerabek : Anaphylaxis. In: Werner E. Gerabek u. a. (Ed.): Encyclopedia of medical history. De Gruyter, Berlin / New York 2005, ISBN 3-11-015714-4 , p. 55.
- Hans Schadewaldt : Idiosyncrasy, anaphylaxis, allergy, atopy. A contribution to the history of hypersensitivity diseases. Opladen 1981 (= Rheinisch-Westfälische Akademie der Wissenschaften, lectures in the humanities , 251).
Web links
Individual evidence
- ↑ U. Müller-Werdan and K. Werdan: Anaphylactic shock. In: Intensivmedizin ecomed-Verlag; Eckart, Forst, Burchardi (editor); 2004, ISBN 3-609-20177-0 .
- ↑ Lifeline: Anaphylactic shock emergency kit for allergy sufferers
- ↑ Insect venom allergy initiative
- ^ Wissenschaft-Online-Lexika: Entry on anaphylaxis in the lexicon of nutrition. Retrieved June 28, 2011.
- ↑ Lothar Kerp: Allergy and allergic reactions. In: Ludwig Heilmeyer (ed.): Textbook of internal medicine. Springer-Verlag, Berlin / Göttingen / Heidelberg 1955; 2nd edition ibid. 1961, pp. 1130-1159, here: p. 1130.
- ↑ See also "Tachyphylaxis" .
- ↑ Hans Bangen: History of the drug therapy of schizophrenia. Berlin 1992, ISBN 3-927408-82-4 , p. 75.
