[Management of angioedema. Guidelines of the Angiology Section of Slovak Medical Chamber (2013)].

Angioedema is defined as a vascular reaction of the deep dermis/mucous and/or subcutaneous/submucosal tissues with localized vasodilatation and increased permeability of blood vessels resulting in tissue swelling. Angioedema can be mediated by bradykinin or mast cell mediators including histamine. Bradykinin-mediated angioedema can occur either on a hereditary (HAE) or acquired (AAE) basis, due to a deficiency/defect of C1 inhibitor (C1-INH) or not. Three forms of HAE have been defined: HAE due to C1-INH deficiency (type 1 HAE, HAE-1), characterized by low antigenic and functional C1-INH levels; HAE due to C1-INH dysfunction (type 2 HAE, HAE-2), characterized by normal (or elevated) antigenic but low functional C1-INH levels; and HAE with normal C1-INH antigenic and functional levels (HAE-3). Acquired C1-INH deficiency refers to patients with angioedema due to C1-INH deficiency on an acquired basis. There are a variety of acquired types of angioedema not due to C1-INH deficiency, and these may be bradykinin mediated (e.g. angiotensin-converting enzyme inhibitor-induced angioedema) or mast cell mediator histamine mediated (e.g. anaphylactic angioedema and urticarial angioedema). In recent years there have been several changes on how we look at the anaphylaxis. The spectrum of trigger factors and diagnostic and therapeutic algorithms has changed significantly. The anaphylaxis is regarded as any sudden severe hypersensitive reaction, which potentially can lead to death. Term anaphylactoid reaction is no more recommended to be used. Drug of first choice is adrenaline/epinephrine administered intramuscularly. Each patient at risk of angioedema should have a written individual rescue plan and knowledge how to use the first aid medicines.