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Sie haben zu viele Anfragen gesendet, sodass Linguee Ihren Computer ausgesperrt hat.University of Mannheim, Mannheim, Germany. Anaphylaxis is an acute systemic reaction with symptoms of an immediate-type allergic reaction which can involve uae whole organism ateroid is potentially life-threatening [ 1 — 3 ]. The definition of anaphylaxis dietary fat testosterone not globally uniform. At present different classification systems are used. In German-speaking countries, the classification extreme steroid use for respiratory diseases here has generally been applied until now. Anaphylactic reactions are the most severe and potentially life-threatening dramatic conditions seen in allergy.
Guideline for acute therapy and management of anaphylaxis
University of Mannheim, Mannheim, Germany. Anaphylaxis is an acute systemic reaction with symptoms of an immediate-type allergic reaction which can involve the whole organism and is potentially life-threatening [ 1 — 3 ]. The definition of anaphylaxis is not globally uniform.
At present different classification systems are used. In German-speaking countries, the classification used here has generally been applied until now. Anaphylactic reactions are the most severe and potentially life-threatening dramatic conditions seen in allergy. Acute treatment is based on international guidelines and recommendations in textbooks. This was subsequently updated and published as a guideline in [ 5 ]. On resolution of the board of directors of the DGAKI of , the anaphylaxis working group was asked to update the guideline.
The members of this working group have met several times, together with experts from other associations such as allergology, anaesthesiology and intensive care medicine, dermatology, pediatrics, internal medicine, otolaryngology, emergency medicine, pharmacology, pneumology and theoretical surgery.
There were consensus conferences in Wiesbaden in September , in Grainau in March , in Munich in January , October and December and finalizing via electronic mail rounds. Case series were of greatest importance, whereas theoretical reflections influenced the assessment only when singular cases, nor case series or experimental investigations could not be used for the evaluation.
As a whole, the number of meaningful studies of anaphylaxis treatment is so low that its management remains empirical in many fields and is often derived from pathophysiological reflections. Anaphylactic reactions may come to a spontaneous standstill at any symptomatic stage, but they may also progress in spite of adequate therapy. This unpredictability makes it difficult to evaluate the effectiveness of therapeutic measures. Observations of a single case do not allow assessments as to whether specific measures were effective.
It is, however, evident that patients received inadequate follow-up care after anaphylaxis due to an insect sting [ 6 , 7 ]. The fact that basic patient care is suboptimal underlines the need for more research as well as the importance of the present guideline.
This guideline is for all doctors and other persons working in the medical field who are concerned with acute treatment, diagnostics and counselling of patients with anaphylaxis. Since anaphylaxis was first described [ 8 ], there have been few exact epidemiological studies on the frequency prevalence and incidence of anaphylactic reactions.
Because of the non-uniform definition see below , a considerable number of undetected cases must be assumed. A limitation of the data on the epidemiology of anaphylaxis is due to the non-uniform ICD coding terms of anaphylaxis.
There are numerous ICD coding terms that may include anaphylaxis. In addition, the definition of anaphylaxis is globally non-uniform [ 9 ]. It has to be clarified in particular whether recurrent cutaneous reactions due to type I allergy should already be considered as anaphylaxis, whether participation of at least two organ systems should be present per definition or whether only the involvement of the organs of the respiratory and cardiovascular systems represent a severe reaction that should be regarded as anaphylaxis.
At present there is neither national nor international consensus regarding this. Published data regarding epidemiology must therefore be evaluated in consideration of these aspects [ 10 ]. One to three anaphylaxis-induced fatalities per year per 1 million inhabitants are estimated [ 12 ].
These numbers imply an increase in anaphylaxis over the last few decades, the cause being unclear. Numbers from the anaphylaxis register of the German-speaking countries and also data from other countries in the world show that foods are the most frequent triggers of anaphylaxis in childhood [ 10 ].
Insect venoms as well as drugs are the most frequent triggers in adults in Germany Tab. In childhood, boys suffer anaphylaxis more frequently than girls with distribution adaptation between the genders occuring after puberty [ 16 ].
The symptoms of anaphylactic reactions are caused by release of different mediators e. However, there is a consensus that histamine plays a central role in anaphylactic reactions. The pathomechanism of anaphylaxis usually represents an immunological reaction, most often an immunoglobulin E mediated allergy. However, specific antibodies of other classes can trigger similar complement-dependent symptoms through the formation of circulating immune complexes immune complex anaphylaxis [ 20 ].
The mechanisms of this non-allergic anaphylaxis comprise G protein-induced, direct release of vasoactive mediators, direct activation of the complement system, interactions with the kallikrein-kinin system, interactions with arachidonic acid metabolism as well as psychoneurogenic reflex mechanisms.
Knowledge on the pathophysiology of these reactions is much more limited than on allergic anaphylaxis. Also the intake of nonsteroidal anti-inflammatory drugs NSAIDs can result in severe anaphylactic reactions due to increased leukotriene formation and facilitated absorption of ingested allergens. Anaphylactic reactions essentially manifest on the skin, in the respiratory tract, gastrointestinal tract, and cardiovascular system. The working group has discussed whether the guideline should be based on a severity classification, as the treatment of anaphylaxis is symptom-related.
The majority voted for a severity classification. There are different severity classifications in the literature [ 7 , 9 , 25 , 26 ]. Each severity classification has advantages and disadvantages. The majority of the group opted to modify the severity classification which is most frequently used in Germany at present [ 26 ]. Anaphylaxis is classified by degrees of severity from I—IV, depending on the intensity of the clinical symptoms Tab. Classification according to the most severe symptom, no symptom is mandatory.
The symptoms of anaphylactic reactions usually begin acutely and may progress very quickly. Thus, symptoms can deteriorate within minutes resulting in death. The reaction may, however, also come to a spontaneous standstill at any stage and regress spontaneously. In a reaction of grade I severity, the further development and dynamics of the reaction are primarily not foreseeable.
The symptoms may occur either simultaneously or sequentially. There may be primarily circulatory reactions without preceding cutaneous or respiratory signs. Occasionally there are protracted or biphasic courses with recurrent symptoms 6—24 hours after successful initial therapy [ 27 ].
Apart from acute onset of symptoms and biphasic courses, delayed anaphylactic reactions may occur where symptoms only begin some hours after exposure. The most striking example of this particular dynamic has been documented for the allergen galactose-alpha-1,3-galactose in mammalian meat allergy and is probably based on delayed release or systemic availability of allergens or their binding sites [ 28 ].
At the beginning of an anaphylaxis, minor prodromal symptoms or signs can appear, like itching or burning of the palms and soles or in the genital area, a metallic taste, fearfulness, headache or disorientation. Young children cannot specifically express these feelings and they may present with symptoms such as restlessness or withdrawal behaviour even before the occurrence of objective signs. These may occur in areas of the skin having had no direct contact with the trigger systemic spread.
In the upper respiratory tract, patients often describe burning, tingling or itching of the tongue or palate as early symptoms. In the oropharynx, swelling of uvula and tongue can be observed.
Clinical signs are a muffled voice, dysphagia with salivation or inspiratory stridor. The possible consequences of laryngeal edema are airway obstruction with life-threatening hypoxia within a short time period. In the lungs, in particular patients with asthma can develop bronchoconstriction and dyspnoea. Clinical signs are wheezing, prolonged expiration and increased respiratory rate.
Bronchial obstruction is the leading symptom in life-threatening reactions especially in children and adolescents. The degree of asthma correlates directly with the severity of the anaphylactic reaction.
Also to a variable extent vasoconstriction can occur, at times resulting in an extreme increase in pulmonary vascular resistance, respiratory arrest and the need for resuscitation.
Pulmonary edema can also occur as a consequence of this permeability disturbance [ 29 — 32 ]. Gastrointestinal symptoms include crampy abdominal pain, nausea, vomiting and diarrhea. There may also be increased intestinal motility with meteorism, the urge to defecate and even involuntary defecation.
Further abdominal symptoms consist of the urge to urinate, micturition as well as uterine cramps. In children, mild oral symptoms or perioral reddening with vomiting may be the only symptoms of food-induced anaphylaxis. Because of vasodilatation and increased vascular permeability, fluid loss into the extravascular space occurs leading to hemoconcentration and hypovolemia, followed by arterial hypotension and tachycardia. Direct cardiac symptoms include arrhythmia, bradycardia or myocardial infarction.
Central nervous system symptoms are restlessness, withdrawal behaviour, headache, seizures, impaired and loss of consciousness. In children, a change in behaviour is often observed, expressed by anxiety or sometimes aggression.
The most frequent triggers of severe anaphylactic reactions are drugs, insect venoms and foods. The ranking of the triggers depends on age and circumstances. In children, foods are very frequent triggers, whereas for adults insect stings or drugs including preparations for allergen-specific immunotherapy and chemotherapeutic agents are more often mentioned Tab. In strongly sensitized persons, anaphylaxis can also be triggered by air-borne allergens or by application to the skin surface [ 33 ].
Anaphylactic symptoms can also occur depending on the combination of various factors, e. A more common form is food-dependent exercise-induced anaphylaxis FDEIA , which is most frequently triggered by wheat flour [ 35 ]. Risk factors which exist independent of the trigger are high age [ 16 ], severe cardiovascular diseases, pre-existing and in particular poorly controlled bronchial asthma, intake of drugs promoting mast cell activation or leukotriene formation e.
In consideration of the trigger-related subgroups of anaphylaxis, there are data for food anaphylaxis showing that here again allergic bronchial asthma is an important risk factor [ 36 ]. The specific trigger may in itself act as a risk factor; it is known, for example, that peanut as a potent allergen is a risk factor for severe reactions [ 37 ]. The clinical symptoms of anaphylaxis are not always characteristic so that diagnosis may be difficult.
In these situations it is especially important to distinguish other conditions from symptoms of an anaphylactic reaction, e. Important differential diagnoses are listed in Tab. After adequate acute treatment, it is helpful to measure mediators in the blood, above all serum tryptase, ideally about one to three hours after the onset of anaphylaxis and — if possible — a comparison to basal serum tryptase should be made.
Serum tryptase can also be measured at a later time, even post mortem [ 38 , 39 ]. In a consensus conference, the following symptoms were regarded as being of specific importance for the diagnosis of anaphylaxis [ 9 ]:. In specific pharmacotherapy, the following substances have proven to be effective:. The most important drug in the acute therapy of anaphylaxis is adrenaline epinephrine.
Administered intravenously, it shows the fastest onset of action of all anaphylaxis drugs. In a patient not in need of resuscitation, immediate intramuscular application of a dose of 0. Compared with intravenous application, the risk of severe cardiac side effects is considerably lower. In case of no response, the injection can be repeated every 5—10 minutes, depending on side effects. Subcutaneous injection of adrenaline is no longer recommended because of insufficient absorption resulting in delayed onset of action.
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13 Aug Pulmonary edema after administration of propofol has rarely been reported. The patient was a smoker and denied drug allergies, use of medications or illicit drugs. He was . Pharmacological interventions for pulmonary edema, Steroids, our understanding of the scope and underlying disease process. () The long-term pulmonary sequelae of prematurity: the rate of familial airway Belik J () Intratracheal N-acetylcysteine use in infants with chronic lung disease. complications of extreme prematurity in mechanically ventilated infants. () Effects of antenatal steroid therapy on mortality and morbidity in very. 6. Juli These conditions include certain types of arthritis, severe allergic reactions, whether the source of the problem is an upper respiratory infection, of CSF AD biomarkers with prednisone treatment of other diseases, and an.