Background
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. In 1994, a position paper of the German Society for
Allergology and Clinical Immunology (DGAKI), was published in the Allergo Journal
as the result of an interdisciplinary consensus conference [4]. This was subsequently
updated and published as a guideline in 2007 [5].
On resolution of the board of directors of the DGAKI of 2009, 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.
In addition to DGAKI members, members of the Association of German Allergologists
(AeDA), the Society of Pediatric Allergy and Environmental Medicine (GPA), the German
Professional Association of Pediatricians (BVKJ), the German Academy of Allergology
and Environmental Medicine (DAAU), the Austrian Society for Allergology and Immunology
(ÖGAI), the Swiss Society for Allergy and Immunology (SGAI), the German Society of
Anaesthesiology and Intensive Care Medicine (DGAI), the German Society of Pharmacology
(DGP), the German Society for Psychosomatic Medicine (DGPM), the German Working Group
of Anaphylaxis Training and Education (AGATE) as well as the patient organisation
German Allergy and Asthma Association (DAAB) were included. There were consensus conferences
in Wiesbaden in September 2009, in Grainau in March 2011, in Munich in January 2012,
October 2012 and December 2012 and finalizing via electronic mail rounds. The recommendations
worked out at the conferences are based on literature searches with assessment of
clinical studies, case series, singular case reports, experimental investigations,
on participants’ experience as well as on theoretical reflections. 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.
Epidemiology of 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-10 coding terms of anaphylaxis. There are numerous ICD-10 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].
Retrospective studies suggest that up to 1 % of patients present to the emergency
department of a maximum care hospital because of an anaphylactic reaction [11]. One
to three anaphylaxis-induced fatalities per year per 1 million inhabitants are estimated
[12].
There are up-to-date studies from the USA, Great Britain and Australia on the epidemiology
of anaphylaxis. They show incidence rates of anaphylaxis of between 7 to 50 per 100,000
/ year [13–15]. 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.
1
), whereby internationally the order varies. In childhood, boys suffer anaphylaxis
more frequently than girls with distribution adaptation between the genders occuring
after puberty [16].
Elicitor
Children
Adults
Food
58 %
16 %
Insect venoms
24 %
55 %
Drugs
8 %
21 %
Pathophysiology
The symptoms of anaphylactic reactions are caused by release of different mediators
(e.g. histamine, prostaglandins, leukotrienes, tryptase, platelet-activating factor,
cytokines, chemokines) from mast cells and basophil granulocytes [17–19], the individual
significance of each of these is not assessed clearly in detail. 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].
There are also a high number of anaphylactic reactions where no immunological sensitization
is detectable; these reactions are called „pseudo-allergic reactions“ [20] or recently
„non-allergic anaphylaxis“ [1]. 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.
In patients with increased basal serum tryptase and/or mastocytosis, anaphylaxis may
be particularly severe [21–23].
Preceding intake of β-adrenoceptor antagonists and ACE inhibitors can lead to a deterioration
of the anaphylactic symptoms [24]. For β-adrenoceptor antagonists, blocking of the
cardiostimulatory effect of adrenaline as well as its mast cell-stabilizing effect
play a role, and, in the case of ACE inhibitors, reduced bradykinin clearence with
resulting marked vasodilatation. 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.
Clinical Symptoms
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.
2
).
Grade
Skin
Abdomen
Airways
Cardiovascular system
I
Itch Flush Urticaria Angioedema
-
-
-
II
Itch Flush Urticaria Angioedema
Nausea Cramps
Rhinorrhea Hoarseness Dyspnea
Tachycardia (> 20/min) Hypertension (> 20 mm Hg syst.) Arrhythmia
III
Itch Flush Urticaria Angioedema
Vomiting Defecation
Laryngeal edema Bronchospasm Cyanosis
Schock
IV
Itch Flush Urticaria Angioedema
Vomiting Defecation
Respiratory arrest
Cardiac arrest
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.
In anaphylaxis most often the skin and mucous membranes are affected with pruritus,
erythema (flush) as well as urticaria and angioedema (Quincke’s edema). 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. Older children, adolescents
and adults can experience “a sense of impending doom“.
In particular the causes of fatal anaphylaxis are airway obstruction and/or cardiovascular
failure, either due to direct cardiac involvement or as a consequence of the microcirculatory
dysfunction with shock; rare causes are disseminated intravascular coagulation or
adrenaline overdose [32].
Allergens and triggers
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.
1
).
The contact with the anaphylaxis trigger most frequently occurs via the oral or parenteral/hematogenous
route. 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.g. allergen exposure together with physical exertion (“exercise-induced anaphylaxis“)
[34], alcohol, mental stress or emotional stress, acute infections or simultaneous
exposure to other allergens as well as concurrent intake of anaphylaxis-enhancing
drugs. This phenomenon is called “augmentation“ or “summation“ anaphylaxis. A more
common form is food-dependent exercise-induced anaphylaxis (FDEIA), which is most
frequently triggered by wheat flour [35].
Risk factors for severe anaphylaxis
There are several risk factors for severe (grade III and grade IV) anaphylaxis. 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.g. NSAID) and
mastocytosis. For insect venom allergy, the intake of β-adrenoreceptor antagonists
and ACE inhibitors, physical and psychological stress as well as an increased basal
serum tryptase are also mentioned [24].
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].
Diagnosis and important differential diagnoses
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.g. other triggers of isolated
urticaria, airway obstruction, vomiting, nausea, diarrhea, restlessness, unconsciousness,
cardiac arrhythmia or cardiac arrest. Important differential diagnoses are listed
in Tab.
3
. 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].
Cardiovascular diseases
_ Vasovagal syncope_ Cardiogenic shock_ Cardiac arrhythmia_ Hypertensive crisis_ Pulmonary
embolism_ Myocardial infarction
Endocrinological diseases
_ Carcinoid syndrome_ Pheochromocytoma_ Thyrotoxic crisis_ Hypoglycemia
Neuropsychiatric diseases
_ Hyperventilation syndrome_ Anxiety/panic attacks_ Dissociative disturbances and
conversion disorders (e.g. globus hystericus)_ Psychoses_ Factitious disorders (Münchhausen
syndrome)_ Somatoform disturbances (e.g. psychogenic dyspnea, „vocal cord dysfunction“)_
Epilepsy_ Coma (e.g. metabolic, traumatic)
Respiratory diseases
_ Status asthmaticus (acute severe asthma without involvement of other organs)_ Acute
obstructive laryngo-tracheitis_ Tracheal/bronchial obstruction (e.g. foreign objects)
Skin diseases
_ Urticaria and hereditary/ acquired angioedemaNote: in physical urticaria extensive
exposure to the respective elicitor can induce anaphylaxis
Pharmacologic/toxic substances
_ Ethanol_ Histaminosis (e.g. scombroid poisoning)_ Opioids (morphine)_ Hoigné-Syndrome
In a consensus conference, the following symptoms were regarded as being of specific
importance for the diagnosis of anaphylaxis [9]:
Sudden occurrence of symptoms on the skin (e.g. acute urticaria, angioedema, flush,
swelling of mucous membranes) in addition to rapid onset respiratory symptoms (e.g.
dyspnoea, wheeze, cough, stridor) or a sudden blood pressure drop or clinical manifestations
thereof (e.g. collapse, tachycardia, incontinence) or
Sudden occurrence of symptoms in two or more of the following organs or organ systems:
skin (e.g. acute urticaria, angioedema, flush, swelling of mucous membranes), gastrointestinal
tract (e.g. abdominal cramps, vomiting), respiratory tract (e.g. dyspnoea, wheezing,
cough, stridor) or circulatory system (e.g. hypotension, collapse, incontinence) after
contact with a probable allergen or anaphylaxis trigger or
Hypotension following contact with an allergen known to the patient or another anaphylaxis
trigger.
Pharmacology of the most important drugs in anaphylaxis treatment
In specific pharmacotherapy, the following substances have proven to be effective:
Vasoactive substances
Adrenaline: The most important drug in the acute therapy of anaphylaxis is adrenaline
(epinephrine). Through the activation of α- and β-adrenergic receptors, adrenaline
functionally antagonises all of the important pathomechanisms of anaphylaxis by vasoconstriction,
reduction of vascular permeability, bronchodilatation, edema reduction and positive
inotropy in the heart. 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 0.3 to 0.5 mg adrenaline (body weight range 30 to 50 kg) to the outer upper
thigh is the drug therapy of first-choice. 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.
If the patient is unstable or during resuscitation, i.e. in case of respiratory and/or
circulatory arrest, adrenaline should be applied intravenously [40]. For this, a dilution
of 1 mg adrenaline in 10 ml NaCl 0.9 %, i.e. a solution of 0.1 mg/ml is administered,
depending on effects and side effects, under continuous control of circulatory parameters.
A continuous infusion of approx. 0.05–1 μg/kg/minute is equally effective. Control
of pulse and blood pressure is mandatory. In patients receiving treatment with β-adrenoreceptor
antagonists and not responding to the repeated injection of adrenaline or other vasoactive
substances (see below), administration of glucagon is recommended [41]. Glucagon,
however, only has an effect on cardiac symptoms.
Additional inhalation of adrenaline after intramuscular application is effective in
the case of laryngeal edema and also in bronchospasm. For this purpose, administration
of adrenaline (e.g. 2 ml of 1 mg/ml) given with oxygen through a nebuliser and respiratory
mask is recommended. Application of inhaled adrenaline cannot replace parenteral administration.
In the case of mainly bronchial obstruction, additional administration of an inhalative
β-adreno-receptor agonist, e.g. salbutamol or terbutaline, at a dose of 2–4 puffs,
is effective. A spacer device should be used in order to improve the efficacy of inhalation
when using an aerosol spray.
In the past, in case of hypotension during pregnancy, administration of ephedrine
instead of adrenaline was sometimes recommended. There is, however, even less information
on ephedrine than on adrenaline. Therefore we also recommend — in agreement with other
authors — the application of adrenaline for anaphylaxis during pregnancy [42].
Even when adrenaline is adequately applied, treatment failure or side effects can
be observed. The increase in cardiac output leads to elevated oxygen consumption and
can be arrhythmogenic, so that, in patients with coronary heart disease, the intravenous
application of adrenaline may cause angina pectoris or a myocardial infarction. In
case of severe life-threatening anaphylaxis there is no absolute contraindication
for adrenaline. The indication should, however, be carefully considered in patients
with pre-existing heart disease.
Other vasoactive substances
Dopamine, noradrenaline and vasopressin are applied in life threatening situations
by emergency doctors and under intensive care conditions with continuous monitoring
of vital signs.
Dopamine: A favourable action profile for the treatment of cardiovascular reactions
is offered by dopamine which affects α and β adrenoreceptors and has a short half-life.
Dopamine leads in low doses, via vascular D1 dopaminergic receptors, to vasodilatation
in the renal, mesenteric and coronary vascular bed [43, 44]. At higher concentrations,
the blood pressure reducing effect by stimulation of the α and β1 receptors prevails.
Bronchodilatation also occurs through activation of the β2 adrenoceptor. It is, however,
less marked than with adrenaline because dopamine is only a partial β2 adrenoceptor
agonist. If adrenaline and volume substitution are insufficient to control symptoms,
dopamine can be administered as a continuous intravenous infusion instead of adrenaline.
The usual dose is 2–15 μg/kg/minute. Application of dopamine is bound to pulse and
blood pressure monitoring. Dopamine is used above all in patients that are receiving
treatment with β adrenoreceptor antagonists.
Noradrenaline: Noradrenaline is a potent α und β1 adrenoceptor agonist and stimulates
the β2-adrenoceptor to a lesser extent than adrenaline so that, at a therapeutic dose,
the bronchodilatatory effect is lower. Therefore an increase in peripheral resistance
and systolic blood pressure prevails. There is little effect on the lung. Noradrenaline
is used especially when the effect of volume substitution and adrenaline/dopamine
is insufficient [45, 46]. Due to its marked vasoconstrictive effect, it should be
administered only as a continuous intravenous infusion under strict blood pressure
and pulse monitoring. The usual dose is 0.02–0.15 μg/kg/minute.
Vasopressin: In anaesthesiological literature, the application of vasopression for
the treatment of severe hypotension is described [47].
Oxygen
In case of manifest cardiovascular or pulmonary reactions, immediate supply of oxygen
via an oxygen mask with reservoir bag, is recommended. Administration of high flow
100 % oxygen is recommended. A laryngeal mask or a laryngeal tube can be helpful.
Only in rare cases will endotracheal intubation by an experienced physician (usually
emergency physician, anaesthesiologist) become necessary.
Volume substitution
An important pathophysiological aspect of anaphylaxis is the resulting hypovolemia
which is treated with adequate volume substitution [48–51]. For severe anaphylactic
reactions, the supply of large amounts of fluid within a short time is necessary.
This can only be achieved through large-bore venous access. If intravenous access
is not possible, a special intra-osseous needle can be inserted preferably into the
tibia. In case of anaphylactic shock, a supply of 0.5–1 liters, and possibly up to
2–3 liters of fluid — depending on the response — in a very short time is required
for adults, for children initially 20 ml/kg body weight.
Primarily, normal saline (NaCl 0.9 %) or balanced electrolyte solutions should be
used. When large quantities of electrolyte solutions are given, they remain in the
intravascular space for a short time only. Therefore, failing stabilization after
the application of larger volumes of electrolytes (> 1 l) the additional application
of colloid volume substitutes can be considered. Gelatine and dextran solutions are
— in spite of their positive qualities — to be viewed cautiously because of their
histamine-liberating potential and the possibility of themselves triggering anaphylaxis
(e.g. dextran without pretreatment with low-molecular hapten dextran).
Hydroxyethyl starch (HES) preparations, such as mean-molecular weight HES (HES 6 %
200/0.5) are the most commonly used volume substitutes in anaphylactic shock. Deposits
in the reticular endothelial system have been observed after infusion of more than
1.5 l HES 200/0.5 in adults [48]. For emergency or intensive care use in unstable
circulatory situations hypertonic, hyperoncotic solutions or mean-molecular weight
HES 130/0.4 in 6 % solution are also available. For short-term infusions the risk
of an possible renal insufficiency is low [52]. In recent literature the use of colloidal
volume substitutes, compared with crystalline solutions in the acute treatment of
shock conditions is being discussed more and more critically [53].
Antihistamines H1 receptor antagonists
The central role of histamine as a mediator of allergic reactions and the efficacy
of H1 antagonists in acute urticaria or rhinoconjunctivitis are evident. Their effects
on circulatory parameters and bronchoconstriction, however, are poorly documented
[54]. Compared to adrenaline, antihistamines show a slower onset of action; however,
they show a favorable benefit/side effect profile in a broad range of indications.
An effect upon the allergic reaction can be assumed and therefore, antihistamines
should be given early in all anaphylactic reactions in order to block the effects
of histamine.
The only H1 antihistamines registered for intravenous application in the acute treatment
of anaphylaxis are the first-generation substances dimetindene (0.1 mg/kg bw) and
clemastine (0.05 mg/ kg bw) with their well-known sedating side effects. Officially
the maximum licensed dose of oral antihistamines is recommended. The expert group,
however, had a consensus that in single selected cases higher doses (up to a maximum
of the fourfold dose of the respective substance) can be given, as has been recommended
for the treatment of chronic urticaria [55]. In higher doses antihistamines, however,
can exert anticholinergic effects leading to tachycardia, dry mouth, gastrointestinal
atony, urinary retention, an increase in ocular pressure up to acute glaucoma attack
as well as irritability and paradoxical excitability [56]. These symptoms should be
kept in mind.
H1 antihistamines of the second generation are not currently licensed for the treatment
of anaphylaxis and are not available for intravenous injection. In spite of this for
emergency oral treatment, the newer more selective H1 antagonists are often recommended;
in placebo-controlled skin test studies they have shown a rapid onset of action [54].
Further studies with newer H1 antihistamines for the treatment of anaphylaxis should
be performed. In particular intravenous preparations of modern non-sedating H1 antagonists
would be helpful.
There is little evidence supporting the efficacy of H2 receptor antagonists in the
treatment of acute anaphylactic reactions. One study reported a reduction of cutaneous
symptoms after additional application of ranitidine compared with H1 antagonists alone
in the treatment of anaphylactic reactions [57]. The prevention of hypersensitivity
reactions by addition of H2 receptor antagonists is better documented; however, this
effect was not analyzed independently from other given medication [58, 59]. There
are single case reports for ranitidine in the treatment of anaphylactic reactions
[60]. We recommend the additional application of H2 receptor antagonists in severe
and treatment-resistant anaphylaxis, since although there is only limited evidence
regarding efficacy, there are no major side effects to be expected [61].
Glucocorticosteroids
Due to their slow onset of action, glucocorticosteroids play a minor role in the acute
phase of anaphylaxis treatment [62]. There are no systematic clinical trials regarding
this indication. However, glucocorticosteroids are effective in the treatment of asthma
and against protracted or biphasic anaphylactic reactions. An unspecific membrane
stabilizing effect within the first 10–30 minutes of application of high dose glucocorticosteroids
(500–1,000 mg) independent of the potency of the glucocorticosteroids has been postulated
in review articles [2,4,62]. When there is no intravenous catheter, glucocorticosteroids
may be applied rectally, especially in small children (e.g. prednisolone suppositories)
or orally.
Treatment
The emergency, symptom-orientated treatment of anaphylaxis has to be carried out rapidly.
A diagram illustrating the treatment steps for physicians and the emergency team has
been published and is updated in the development of this guideline (Fig.
1
) [63].
At first further allergen exposure should be stopped if possible. In some situations
(e.g. intravenous infusion) this can be done easily without losing time. The application
of a tourniquet and/or the subcutaneous injection of epinephrine surrounding a local
allergen depot (e.g. a wasp sting or injection site of specific immunotherapy) is
no longer recommended due to the limited therapeutic benefit and risk of losing time
for more important measures. Further assistance should be called in order to guarantee
adequate medical care. Each physician should have emergency equipment for the treatment
of anaphylactic reactions (Tab.
4
) in his practice. A teamapproach with the opportunity to delegate procedures is advisable.
Stethoscope, blood pressure monitor
Tourniquet, syringes, in-dwelling catheter, infusion set
Oxygen with mask/nasal cannula
Guedel-tube, bag valve mask, suction unit, intubation set
Adrenaline for injection
H1 antihistamines for intravenous injection
Infusion solutions (0.9 % NaCl solution, balanced electrolytes/ colloids)
Glucocorticosteroids for intravenous injection
Bronchiodilator (rapidly acting β 2 adrenoreceptor agonist for inhalation or intravenous
injection)
Automatic external defi brillator (optional)
Pulse oximeter (optional)
First, a quick history and basic physical examination have to be done (Fig.
1
). This includes:
Check of vital signs (spontaneous movements and breathing)
Evaluation of pulse and blood pressure (strength, frequency, regularity)
Evaluation of breathing (dyspnea on speaking, inspiratory or expiratory stridor, wheezing,
optional: auscultation, measurement of the peak flow using a mechanical peak flow
meter, pulse oximetry),
Inspection of visible skin and mucous membranes,
Questioning for further complaints, e.g. nausea, impulse to vomit, headache, sternal
pressure, disturbance of vision, pruritus),
Questioning for known allergies.
Regarding vital parameters, possible alarm values are listed in Tab.
5
. These examinations should be repeated regularly in the course of acute management.
Alarm thresholds depending on age
upto 1 year
1–5 years
6–14 years
> 14 years
Pulse rate (/min)
> 160
> 130
> 120
>110
Blood pressure (systolic, mmHg)
< 50
< 60
< 60
< 70
Respiratory rate (/min)
> 40
> 35
> 30
> 25
Oxygen saturation (%)
< 92
< 92
< 92
< 92
*These values show a high individual variability and should only be regarded as approximate
information. There are no studies from larger cohorts.
Smaller children can initially be examined in the arms of the parents. It is important
to calm the child and the parents in order to allow adequate examination and treatment.
When the child is fidgety, inspection of the mouth or auscultation may be difficult
or even impossible. Irritation by the use of a spatula may increase airway obstruction
and should be avoided. Clinical signs of airway obstruction like prolonged expiration,
in- or expiratory stridor, wheezing, salivation, retraction of the thoracic wall and
constriction nasal alae should be looked for.
Evaluation of severity
Based on the examination the degree of severity of the anaphylaxis should be evaluated
and the most threatening symptom of anaphylaxis identified (Fig.
1
). The most life-threatening symptom of anaphylaxis should be treated with priority.
This may lead to 6 possible scenarios:
Anaphylaxis with cardiac or circulatory arrest (anaphylaxis grade IV)
Anaphylaxis with predominant cardiac and circulatory reaction (anaphylaxis grade II/III)
Anaphylaxis with predominant obstruction of upper airways (anaphylaxis grade II/III)
Anaphylaxis with predominant obstruction of lower airways (anaphylaxis grade II/III)
Anaphylaxis with predominant gastrointestinal involvement (anaphylaxis grade II)
Anaphylaxis with systemic generalized skin manifestations and subjective symptoms
(anaphylaxis grade I).
Positioning
Immediately after examination, the patient should be positioned according to symptoms.
Horizontal positioning and avoidance of further physical exercise (walking or trying
to sit up) are the basic strategies. Depending on the situation the positioning can
be varied. Getting up and physical exercise should be avoided because of possible
further aggravation of anaphylaxis (as with co-factors). When consciousness is impaired
especially in a preclinical situation, the recovery position is preferred. For improvement
of the hemodynamic situation the patient may be placed in the Trendelenburg position
(elevated legs). In situations with predominant respiratory symptoms a (half) sitting
position is preferable. In the treatment of children actions should not be forced
in order to avoid increasing distress.
Anaphylaxis with cardiac or circulatory arrest
Cardiopulmonary resuscitation with cardiac massage and aided ventilation in a ratio
of 30 :2 must be started (Fig.
1
). An automatic defibrillator should be connected. And in case of ventricular fibrillation
early defibrillation has to be initiated. For further pharmacotherapy an intravenous
or intraosseous catheter is mandatory. Intravenously applied adrenaline is the substance
of choice. 1 ml adrenaline (1 mg/ml) is diluted in a ratio of 1 : 10 to a volume of
10 ml (0,1 mg/ml) and given as a 1 mg bolus (= 10 ml) in 2–5 minute intervals until
circulation is stabilized. For sufficient oxygenation the airway must be secured.
This can be done via endotracheal intubation. Alternatively a laryngeal mask or a
laryngeal tube or a combined tube can be used depending on the experience of the physician.
The flow of the inspiratory oxygen (FiO2) should be above 0,8. For this, the application
of high-flow oxygen with a reservoir bag is necessary. Based on the pathophysiology
of anaphylaxis, forced volume substitution and high dose anti-allergic treatment (antihistamines,
glucocorticosteroids) are mandatory for the correction of hypovolemia and successful
resuscitation. Immediate transfer to an intensive care unit is advisable (Tab.
6
).
Substance
Route of application
< 15 kg bw
15–30 kg bw
30–60 kg bw
> 60 kg bw
Adrenaline
Intravenous, bolus1
0.1 ml/kg bw (from 1 mg/10 ml) 1
0.1 ml/kg bw (from 1 mg/10 ml) 1
0.05–0.1 ml/kg bw (from 1 mg/10 ml) 1
0.05–0.1 ml/kg bw (from 1 mg/10 ml) 1
Adrenaline
Continuous infusion
0.05–1.0 μg/kg/min
0.05–1.0 μg/kg/min
0.05–1.0 μg/kg/min
0.05–1.0 μg/kg/min
Adrenaline
Inhaled via nebulizer
2 ml2
2 ml2
2 ml2
2 ml2
Dimetindene
Intravenous
1 ml3
2–3 ml3
4 ml3
8 ml3 oder1 ml/10 kg bw
Prednisolone
Intravenous
50 mg
100 mg
250 mg
250–1000 mg
Salbutamol Terbutalin
Inhaled
2 puffs DA per spacer
2 puffs DA per spacer
2–4 puffs DA per spacer
2–4 puffs DA per spacer
Reproterol4
Continuous infusion
0,1 μg/kg/min
0,1 μg/kg/min
0,1 μg/kg/min
0,1 μg/kg/min
Volume
Bolus (0,9 % NaCl)
20 ml/kg bw
20 ml/kg bw
10–20 ml/kg bw
10–20 ml/kg bw
Volume
Infusion (electrolyte solution)
1 to 2 ml/kg/min
1 to 2 ml/kg/min
1 to 2 ml/kg/min
1 to 2 ml/kg/min
Oxygen
Inhaled
2 to 10 l/min
5 to 12 l/min
5 to 12 l/min
5 to 12 l/min
1
For the application of a bolus a 1 mg/ml adrenaline solution is diluted (1 ml plus
9 ml 0.9 % NaCl) to a final concentration of 0.1 mg/ml);
2
For inhalation the original concentration is used (1 mg/ml);
3
of the (original) concentration of 1 mg/ml (1 ml = 1 mg);
4
Reproterol can also be given as bolus bw, body weight
Anaphylaxis with predominant cardiovascular reaction
The immediate action is intramuscular injection of epinephrine, especially when there
is no intravenous catheter (Fig.
1
, Tab.
6
). Epinephrine autoinjectors for self-treatment of patients can be helpful in such
situations due to their rapid application. The standardized adrenaline autoinjector
doses of between 0,3 mg and 0,15 mg are feasable. When the response is insufficient
a further intramuscular injection of epinephrine can be repeated after approx. 5 minutes.
The application of oxygen with the aim to increase the inspired oxygen content (FiO2)
above 0,5 is recommended. This can be achieved using an oxygen mask with a reservoir
bag; a nasal cannula has only a limited effect on FiO2.
In all forms of altered consciousness, the patient may vomit and this should be accounted
for when positioning. The mouth can be opened with the Esmarch hand maneuver and the
oral cavity inspected for vomitus that should be removed. A suction unit is helpful.
For further treatment an intravenous catheter is mandatory (Tab.
6
). Failing this, an intraosseus catheter is indicated. The major therapeutic goal
is the correction of a relative hypovolemia. Forced volume substitution of an electrolyte
solution (5–10 ml/kg bw within 5 minutes) is mandatory. The application of such volumes
requires a large bore intravenous cannula (> 8 Gauge) or several venous catheters.
The application of colloidal volume substitutes in the phase of forced volume substitution
is a common emergency medical measure.
Antiallergic substances (antihistamines [beware of anticholinergic side effects] and
glucocorticosteroids) should be used in high doses (Tab.
6
). In persisting or imminent shock the fractionated intravenous/interosseus or intramuscular
application of adrenaline is indicated. Continuous monitoring of blood pressure and
pulse are necessary. Other sympathomimetic substances like dopamine or noradrenalin
may be given as a continuous infusion via a pump system under monitoring of experienced
physicians.
Anaphylaxis with predominant obstruction of the upper airways
Typical signs are due to swellings in the region of the upper airway. This can present
with a clinically visible swelling of the tongue or uvula, dysphonia or inspiratory
stridor. These situations can be life-threatening due to obstruction of the larynx.
Immediate measures in this case are the intramuscular injection of adrenaline and
application of oxygen (Fig.
1
). The administration of inhaled adrenaline is indicated (Tab.
6
, Tab.
7
). In the case of insufficient response to these therapeutic measures, coniotomy may
be required.
Substance
Route of application
< 15 kg bw
15–30 kg bw
> 30–60 kg bw
> 60 kg bw
Adrenaline
Intramuscular
0.01 ml/kg bw (1 mg/1 ml)
0.01 ml/kg bw (1 mg/1 ml)
0.01 ml/kg bw (1 mg/1 ml)
0.01 ml/kg bw (1 mg/1 ml)
Adrenaline
Autoinjector i.m.
see i.m.
150 μg
300 μg
300–600 μg
Adrenaline
Inhaled via nebulizer
2 ml2
2 ml2
2 ml2
2 ml2
Adrenaline
Intravenous bolus1
0.1 ml/kg bw (of 1 mg/10 ml) 1
0.1 ml/kg bw (of 1 mg/10 ml) 1
0,05–0,1 ml/kg bw (of 1 mg/10 ml) 2
0,05–0,1 ml/kg bw (of 1 mg/10 ml) 2
Dimetindene
Intravenous
1 ml3
1 ml/10 kg bw3 (max. 4 ml)
1 ampule = 4 ml3
1–2 ampule = 4–8 ml3 (1 ml/10 kg bw)
Prednisolone
Intravenous
50 mg
100 mg
250 mg
500–1000 mg
Salbutamol Terbutalin
Inhaled
2 hubs DA per spacer
2 hubs DA per spacer
2–4 hubs DA per spacer
2–4 hubs DA per spacer
Volume
Bolus (NaCl 0.9 %)
20 ml/kg bw
20 ml/kg bw
10–20 ml/kg bw
10–20 ml/kg bw
Volume
Infusion (Ringer solution)
1 to 2 ml/kg/min
1 to 2 ml/kg/min
1 to 2 ml/kg/min
1 to 2 ml/kg/min
Oxygen
Inhaled
2 to 10 l/min
5 to 12 l/min
5 to 12 l/min
5 to 12 l/min
1
For the application of a bolus a 1 mg/ml adrenaline solution is diluted (1 ml plus
9 ml 0.9 % NaCl) to a fifi nal concentration of 0.1 mg/ml);
2
For inhalation application the original concentration is used (1 mg/ml)
3
of a (original) concentration of 1 mg/ml (1 ml = 1 mg) bw, body weight
Anaphylaxis with predominant bronchial obstruction
Broncial symptoms belong to the most common symptoms of severe anaphylaxis. In all
potentially life-threatening situations the immediate intramuscular application of
adrenaline is indicated. Also topical bronchodilatory treatment is of central importance
(Fig.
1
). Several short acting β2 sympathomimetics (e. g. salbutamol, terbutaline) are available
for the treatment of bronchial obstruction (Tab.
6
, Tab.
7
).
It must be considered that some anaphylaxis patients are not experienced in inhalation
therapy and may need the help of a spacer device in the case of aerosol sprays or
continuous aerosol application (aerosol masks with a pressure/oxygen attachment or
electric nebulizers). In the meantime practical battery-based spray nebulizers are
available which can be used in paramedical and preclinical situations. Should more
intensive therapy be required the intravenous application of adrenaline or injectable
β2 sympathomimetics (terbutaline s. c. or reproterol i. v.) are possible (Tab.
6
). In the case of status asthmaticus, when muscular exhaustion occurs, artificial
ventilation may be necessary [64].
Anaphylaxis with predominant abdominal symptoms
Abdominal symptoms are treated in the same way as anaphylaxis with predominant skin
symptoms (Fig.
1
). Only in the case of insufficient response to systemically applied antiallergic
substances do gastrointestinal symptoms require specific treatment. Nausea, vomiting,
as well as abdominal colic represent the relevant symptoms. Antiemetics like metoclopramide,
antihistamines and dimenhydrinate or the application of a serotonin (5 HTR3) antagonist
(e. g. ondansetron) can be considered. For abdominal cramps the intravenous application
of butylscopolamine may have alleviating effects.
Anaphylaxis with predominant skin manifestations
The application of an intravenous catheter is the first measure of choice. It is recommended
to keep the catheter open by infusion of electrolyte solutions. Anti-allergic substances
like dimetindene and glucocorticosteroids should be given in the usual dose (Fig.
1
, Tab.
7
).
Management of therapy control
The observation of the anaphylaxis patient until he/she is in definite long-lasting
remission is crucial (Fig.
1
). The possibility of a biphasic course of anaphylaxis has to be kept in mind. Therefore
in all severe anaphylactic reactions (grade II grade II and higher) in-patient hospital
observation is indicated. In anaphylaxis with life-threatening systemic reactions
monitoring in an intensive care unit is recommended. On discharge the indication for
the prescription of an emergency set for self-treatment (adrenaline auto-injector,
antihistamines, glucocorticosteroids and possibly a topical bronchodilatory aerosol
spray) should be considered. The practical use of the emergency equipment for self-treatment
— especially the application of the epinephrine autoinjector — should be trained via
educational programs (Tab.
8
; see below). The referral to an allergist for further diagnostic work-up and possible
long-term therapy is necessary. In order to gather information on triggers, associated
circumstances and co-factors of anaphylaxis, an anaphylaxis registry has been installed
in Germany where physicians can report severe anaphylactic reactions online (www.anaphylaxie.net).
Substance
Route of application and dosage
Adrenaline
Autoinjector for intramuscular application, adapted to body weight:> 15 kg 150 μg
adrenaline> 30 kg 300 μg adrenaline
H1 antihistamine
According to age and preference of patients as liquid or fast-melt tablet. The licensed
daily dose of the respective antihistamine is recommended as single dose. Dimetindene
drops can be taken orally in a dosage adapted for bodyweight and corresponding to
the intravenous dose.
Glucocorticosteroid
According to age and preference of the patient oral or rectal (tablets or liquid)
with 50–100 mg Prednisolone equivalent.
Optional
In patients with bronchial asthma: β2 adrenoceptor agonists When airway obstruction
can be expected an adrenaline preparation for inhalation with spray head (to be ordered
especially from the pharmacist)
Note: “The emergency set for self-help” should contain written instructions for the
application of its constituents (e.g. anaphylaxis-passport and/or anaphylaxis-emergency
plan)
Special considerations in childhood
With regard to dosing of certain drugs in the treatment of anaphylaxis the particular
dosages for children have to be considered.
Patient management and self-medication
Target group
Each patient who has suffered from an anaphylaxis must be informed about the most
important behavioral steps that may help in the prevention and treatment of anaphylaxis.
This is particularly important for patients with an increased risk of anaphylaxis
like adults with mastocytosis or a prognostically significant symptom constellation.
This is equally important when the patient successfully undergoes allergen-specific
immunotherapy (ASIT), e.g. against insect venoms.
Self-medication (“emergency set for self-help”)
Basically all patients who have survived an anaphylaxis and cannot avoid with certainty
the elicitor as well as all adult patients with mastocytosis should be prescribed
an “emergency set for self-help” [65, 66]. In Germany, Austria and Switzerland commonly
the following drugs are included in the emergency set: an adrenaline autoinjector,
H1 antihistamine, glucocorticosteroid and for patients with asthma, an inhaled bronchodilator
(Tab.
8
). Each patient with an “emergency set for self-help” must be reminded to always carry
the set with him/her. He/she must be informed about the correct storage and shelf
life of the substances as well as possible sedative side effects caused by older antihistamines
(influence on driving performance). Patients as well as persons in their social network
— in the case of children parents and caretakers — must be instructed in the use of
the medication. For this standardized anaphylaxis emergency plans are available.
Several adrenaline autoinjectors preparations, that apply various single doses (150
μg for patients of 15–30 kg bw, 300 μg for patients over 30 kg bw), are available
for intramuscular injection. There is information, that in otherwise healthy children
with a body weight between 10 and 15 kg, the dose of 150 μg is not hazardous. Parents
must be informed about off-label use in this indication. The available adrenaline
autoinjectors differ in their practical administration: Patients receiving a second
or subsequent autoinjector, should be prescribed a preparation requiring the same
administration technique. In order to train patients and their social environment
in the application of the autoinjector, it is helpful to give them a dummy (without
needle) and to motivate them to practice frequently.
In the selection of an H1 antihistamine, the ease with which it can be swallowed and
individual preferences should be considered regarding the application form (drops
for small children, tablets or fast-melt tablets for older children or adults). If
difficulty in swallowing prevails (laryngeal angioedema), liquid applications are
to be preferred. The same criteria are valid for glucocorticosteroids, whereby rectal
application should also be considered.
In asthma patients, additional inhaled β receptor agonists should prescribed and when
there is a history of laryngeal edema adrenaline for inhalation.
Patients supplied with an emergency set for self-help must be shown how to administer
the medication and also receive written information regarding this. Not all patients
having suffered an immediate-type allergic reaction need an emergency set or autoinjector.
There is no need, when the elicitor is known and easily avoided like in drug-induced
anaphylaxis. Also after allergen-specific immunotherapy with insect venom, patients
without additional risk factors, have no increased risk for anaphylaxis compared to
the normal population. It is therefore not compulsory for these patients to continuously
carry self-medication with them. Indications for the prescription of an adrenaline
autoinjector are listed in Tab.
9
. Occasionally (e.g. very severe anaphylaxis, high body weight, mastocytosis, long
distance to medical care) the prescription of a second autoinjector is advisable.
_ Patients with a systemic allergic reaction and bronchial asthma (even without a
history of anaphylaxis)
_ Progressive severity of symptoms of a systemic allergic reaction
_ History of previous anaphylactic reactions to elicitors which cannot be avoided
with certainty
_ Systemic allergy to potent allergens e.g. peanuts, tree nuts, sesame
_ High degree of sensitization, e.g. patients who react to even minute amounts of
allergen
_ Adults with mastocytosis (even without a history of anaphylaxis)
In addition to the emergency set for self-help an “anaphylaxis passport“ should be
issued which, apart from the elicitors, also contains the dosage of drugs and application
of the drugs dependent upon the reaction.
Practical emergency management
Most anaphylactic emergencies occur at home. Therefore information on emergency self-management
has to include all measures that have to be performed by the patient him-/herself
or by his/her immediate surroundings. The patient should be trained in
the recognition of an anaphylactic reaction
symptom-orientated self-medication
correct positioning
making an emergency call (telephone no. 112 in D and A, 144 in CH). The word “anaphylaxis/anaphylactic
shock“ should be mentioned first, the conversation should then be guided by the rescue
centre.
Potential suspected elicitors (foods, insects, drugs) should be preserved if possible.
Self-medication should be taken depending on symptoms and certainty of allergen contact.
It is essential that patients receive information on when to take which medications
as here often an uncertainty prevails in patients and their relatives. When there
has been a definite contact with an elicitor of anaphylaxis (e.g. insect sting without
preceding allergen-specific immunotherapy or consumption of allergy-inducing foods
or intake of allergy-eliciting drugs), the anaphylaxis emergency plan (Fig.
2
]) must be followed. The immediate application of oral drugs is recommended even if
the patient is asymptomatic. The emergency plan and anaphylaxis passport are important
aids (Fig.
2
).
Long-term therapy and prevention management
After an attack of anaphylaxis, allergy diagnostics should be performed. The identification
of the elicitor, the targeted issuing of an anaphylaxis passport and individual counseling
regarding risks and dangers are the necessary basis for all preventive measures (Tab.
10
). Diagnostics comprise all methods allowing the doubtless identification of an elicitor.
Relevant risk factors for anaphylaxis (e.g. asthma, mastocytosis or medication with
certain drugs) should be identified and their significance explained to the patient.
If possible, allergen-specific immunotherapy should be started [24]. In the case of
recurrent anaphylactic reactions regular monitoring and long-term pharmacotherapy
(e.g. anti-IgE, omalizumab) should be considered [67].
A) Prevention
1. Issuing of an anaphylaxis passport und anaphylaxis emergency plan
2. Emergency set, anaphylaxis-passport and mobile phone should always be at hand
3. Knowledge of the symptoms of anaphylaxis and being able to distinguish them from
other symptoms (e.g. fear)
4. If possible autonomous training with the adrenalin-autoinjector (dummy without
needle and drug) to be repeated every 3–6 months (cave: do not mix up with the “real”
autoinjector!)
5. Shelf life of substances has to be checked regularly. For the Adrenalin-autoinjector
the reminder service of the producing company can be used.
6. Inform the social network: organize support, delegate tasks for emergency situation
(emergency call, application of drugs, receiving the emergency physician etc.)
7. Possibly further counseling, information material and exchange with other patients
via patient organizations (e.g. Deutscher Allergie- und Asthmabund daab, mastocytosis
self help group, anaphylaxis education in small groups according to anaphylaxis group
education and training AGATE in Germany)
B) Emergency self-treatment
8. Application of the emergency set (see Anaphylaxis-passport / Anaphylaxis emergency
plan)
9. Positioning
a) with predominant heart and cardiovascular symptoms: lying down, legs up (shock
positioning)
b) with predominant respiratory symptomatology; sitting (“coachman position”)
c) when there is unconsciousness: recovery position
10. Emergency telephone number: EU 112 (CH 144), the word “anaphylaxis/anaphylactic
shock” should be mentioned fi rst, the conversation should be guided by the rescue
central office
11. Ask for help and support from the social surrounding
Elicitor-specific prevention
Patients with food allergy as elicitor of anaphylaxis should get complete information
and nutritional counseling regarding the identification and possible avoidance from
the eliciting food by an experienced nutritionist (www.ak-dida.de, www.daab.de). This
should comprise information regarding alternative food choises and advice on preventing
potential nutritional deficiencies when consequent avoidance of the culprit food is
necessary. In particular patients should be informed about recent food declaration
regulations and their implications, in order to allow for the low risk purchase of
foods e.g. at the supermarket and when eating out. In patients with insect venom allergy
precautionary strategies for the avoidance of repeated stings have to be discussed;
in patients with drug allergy the risk of cross-reactions to related substances and
the problem of synonyms should be mentioned.
Counseling, educational programs and helpful tools
In order to communicate all the necessary theoretical and practical information, educational
programs as they have been developed by the “Arbeitsgemeinschaft Anaphylaxie Training
und Edukation (AGATE)“ (Working Group Anaphylaxis Education and Training), have proven
helpful [68, 69]. Various target groups (adult patients, parents of children at risk
of anaphylaxis, children, adolescents, child care workers and teachers) are trained
in interdisciplinarily guided group sessions on how to behave in case of anaphylaxis.
Equally, seminars for education of “anaphylaxis trainers“ (train-the-trainer seminars)
are offered (www.anaphylaxieschulung.de). Following allergy diagnostics it is helpful
to inform patients and their relatives of patient organizations (www.daab.de, www.mastozytose.de)
which are experienced in the further counseling of patients with regard to coping
with the disease in everyday life. They also provide information material and helpful
tools such as restaurants cards, preprints of relevant travel documents, liability
exclusion and cards with emergency telephone numbers.