• Dinko Milavec and Ino Husedzinović.
• Klinika za anesteziologiju, reanimatologiju i intenzivno lijecenje, Klinicka bolnica Dubrava, Zagreb.
• Lijec Vjesn. 2006 Sep 1; 128 (9-10): 317-21.

AbstractThe incidence of anaphylactic reactions during anesthesia is between 1:5000 and 1:25000 anesthetics. During the IgE-mediated anaphylactic reaction mast cells release proteases such as tryptase, histamine and vasoactive mediators. The release of mediators from the mast cells and basophils is responsible for the immediate clinical manifestations of anaphylaxis. Anaphylactoid reactions can be caused directly by a release of histamine and other mediators from mast cells and basophils and they don't depend on interaction of IgE antibodies with antigen. The most frequent agents that cause anaphylactic and anaphylactoid reactions during anesthesia are neuromuscular blocking agents (among them the highest percent refers to rocuronium and succinylcholine), some general anesthetics, antibiotics, blood and blood products, opioids and latex. Increased tryptase concentration in serum is a marker for systemic mast cell activation. Skin tests (in vivo) are used for verification of specific hypersensitivity to drugs in patients after anaphylactic reaction. In vitro tests prove the presence of specific IgE antibodies for drugs. The plan for the treatment of anaphylactic reactions must be established before the event. Airway maintenance, 100% oxygen administration, intravascular volume expansion and epinephrine are essential to treat the hypotension and hypoxia that result from vasodilatation, increased capillary permeability and bronchospasm. As soon as the diagnosis has been made the adrenalin should be given intravenously 1 to 3 ml of 1:10000 aqueous solution (0.1 mg/ml) over 10 minutes. Prevention is possible with methylprednisolone 125 mg i.v. 1 hour before administering of anesthetics and neuromuscular blocking agents with or without antihistaminic chlorpiramine-chloride 1 amp i.v. few minutes before anesthesia.

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