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Dtsch Arztebl Int. 2018 Aug; 115(31-32): 528–534.

Published online 2018 Aug 6. doi: 10.3238/arztebl.2018.0528

PMCID: PMC6131363

PMID: 30149833

Adrenaline in the Acute Treatment of Anaphylaxis

Johannes Ring, Prof. Dr. med. Dr. phil.,1,* Ludger Klimek, Prof. Dr. med.,2 and Margitta Worm, Prof. Dr. med.3

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Abstract

Background

Anaphylaxis is the most serious manifestation of an immediate allergic reaction and the most common emergency event in allergology. Adrenaline (epinephrine) is the mainstay of acute pharmacotherapy for this complication. Although epinephrine has been in use for more than a century, physicians and patients are often unsure and inadequately informed about its proper administration and dosing in everyday situations.

Methods

This review is based on pertinent publications from the period 1 January 2012 to 30 September 2017 that were retrieved, on the basis of the existing guidelines of 2007 and 2014, by a PubMed search employing the keywords “anaphylaxis treatment,” “allergic shock,” “adrenaline,” and “epinephrine,” as well as on further articles from the literature.

Results

Adrenaline/epinephrine administration often eliminates all manifestations of anaphylaxis. The method of choice for administering it (except in intensive-care medicine) is by intramuscular injection with an autoinjector; this is mainly done to treat reactions of intermediate severity. The injection is given in the lateral portion of the thigh and can be repeated every 10–15 minutes until there is a response. The dose to be administered is 300–600 µg for an adult or 10 µg/kg for a child. The risk of a serious cardiac adverse effect is lower than with intravenous administration. There have not been any randomized controlled trials on the clinical efficacy of ephinephrine in emergency situations. The use of an autoinjector should be specially practiced in advance.

Conclusion

The immediate treatment of patients with anaphylaxis is held to be adequate, yet major deficiencies remain in their further diagnostic evaluation, in the prescribing of emergency medications, and in patient education. Further research is needed on cardiovascular involvement in anaphylaxis and on potential new therapeutic approaches.

Anaphylaxis is the maximal variant of an acute life-threatening immediate-type allergy and represents the most common and often life-threatening emergency situation in allergology. In contrast to hay fever, asthma, and atopic eczema (atopic dermatitis), few reliable epidemiological studies exist of the prevalence rates of anaphylactic reactions (1).

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Background

In tandem with the general increase in allergic disorders in the population, anaphylactic reactions have become more common, not only in Europe (2– 4), but also in the USA and Asia (5– 7), for example from 16/100 000 person-years in 2008 to 32/100 000 person-years in 2014 (5). With a total prevalence of 42/100 000 person-years in the period from 2001 to 2010, Lee et al. observed an annual increase of 4.3% and, for food-induced anaphylaxis, of 9.8% (6).

In particular, food-induced anaphylaxis in children has increased—for example, from 41/100 000 emergency admissions in 2007 to 72/100 000 such admissions in 2012 (7).

Often, patients with allergic rhinitis (hay fever) also react to allergens that occur in foodstuffs and pollen grains (“pollen-associated food allergies”).

A classic example are people with allergies to birch pollen, who also react with anaphylaxis to hazelnuts, because they have developed IgE antibodies to the major birch pollen allergen Bet v 1, which occurs in many foodstuffs.

Reactions to Bet v 1 homologous proteins are altogether common, but they rarely trigger severe reactions (8).

In view of the numerous triggers and the multiple possibilities for exposure over a lifetime, lifetime prevalence rates of anaphylaxis in the population have been estimated to be 0.3–15%; in some studies this also includes milder reactions, such as externally triggered acute urticaria (9– 11).

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Methods

On the basis of the available guidelines from 2007 and 2014 we conducted a selective literature search in PubMed, using the search terms “anaphylaxis treatment”, “allergic shock”, “adrenaline”, and “epinephrine” for the period from 1 January 2012 to 30 September 2017. We also took recourse to literature we ourselves collected over time.

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Clinical symptoms

Anaphylactic reactions are accompanied by a multitude of symptoms affecting different organs, which sometimes occur in succession and sometimes simultaneously—but not necessarily always to the same degree.

In most cases (80–90%), the reactions start with subjective general symptoms and skin manifestations (for example, urticaria/hives 62%, angioedema 53%), sometimes accompanied by formication on the palms of the hands and soles of the feet. Advanced symptoms include nausea of the gastrointestinal tract in 24% of those affected, colic-type pain in 16%, vomiting in 27%, and diarrhea in 5%.

The respiratory tract is affected in 49%. Those affected experience dyspnea, either as a narrowing of the upper airway in the sense of laryngeal edema or as asthmatic bronchial constriction (35%).

Anaphylaxis can affect the cardiovascular system—for example, by triggering tachycardias or blood pressure fluctuations in up to 42% of cases. These can be so comprehensive that anaphylactic shock may ensue (12– 15) (box).

BOX

The most important symptoms of anaphylaxis*

Subjective general symptoms (known in the past as prodromal symptoms)

Restlessness

Abnormal tiredness in children

Paresthesias or itching of palms, soles of feet, or in anogenital region

Metallic or fishy taste in the mouth

Visual disturbances

Feelings of anxiety

Skin

Generalized pruritus

Disseminated weals (urticaria, hives)

Circumscribed tissue swellings (angioedema, e.g. of the eyelids, lips)

Episodic reddening (flushing)

Gastrointestinal tract

Nausea, vomiting

Stomach cramps, colic

Diarrhea, voiding of feces and/or urine

Airways

Rhinoconjunctivitis

Dyspnea

Wheezing

Asthma attack

Blocking of upper trachea, glottal edema (a feeling of obstruction of the throat)

Respiratory arrest

Cardiovascular system

Palpitations and tachycardia

Drop in blood pressure

Collapse, circulatory shock, cardiac arrhythmia

* modified from (1, 9, 12, 15, 26)

Anaphylaxis can affect the same patient to different degrees of intensity, which is considered in the classification into grades of clinical severity (16, 17).

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Pathophysiology

During the trigger phase of anaphylaxis, mast cells and basophils, which release highly active mediator substances, are of central relevance. The best known substance is histamine (18). Furthermore, eicosanoids—such as leukotrienes and prostaglandins—but also platelet activating factor (PAF) have important roles, which are, however, not fully understood just yet.

Further to activation by antibodies, anaphylaxis can be triggered non-immunologically by direct mediator release or complement activation.

The causes of a fatal outcome are mostly (19, 20):

Circulatory shock

Cardiogenic shock as a result of cardiac arrest (also arrhythmia, myocardial infarction)

Obstruction of the upper airway (laryngeal edema)

Severe asthma attack with bronchoconstriction.

Triggers and allergens

The most important triggers of anaphylaxis in adults are insect venom, foods, and medicines, whereas in children, it’s foods (table 1).

Table 1

Common triggers of anaphylaxis*

Insect venom (n = 2074)Wasp1460Bee412Hornet93Bumblebee5Horsefly4Mosquito4Foods (n = 1039)Pulses (including peanut)241Animal proteins225Nuts199Grains101Fruits65Vegetables63Herbs/spices55Additives13Others17

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* The data come from an anaphylaxis registry. which collects voluntary notifications from the German-speaking region. They therefore do not represent a population-based epidemiological data collection

(modified from [16])

In addition, so called non-specific summation or augmentation factors are relevant, if a reaction is triggered only after simultaneous effects of other, often non-specific factors plus contact with the allergen (1, 21– 24), as for example:

Physical exercise/exertion

Administration of medications (acetylsalicylic acid, beta blockers, angiotensin converting enzyme [ACE] inhibitors, and others)

Acute infections

Psychological stress

Alcohol use

Simultaneous exposure to different allergens.

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Acute treatment

The basic principles of emergency treatment have been described in national and international guidelines (14, 25, 26).

General measures

General measures include:

Interrupting delivery of the allergen

Positioning the patient in a way that is appropriate for their symptoms

Diagnostic evaluation of vital signs

Prompt insertion of an intravenous cannula and administration of fluids as required

Providing oxygen and appropriate cardiopulmonary resuscitation if required (27).

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Medication therapy

Adrenaline/epinephrine is of central importance in the setting of pharmacotherapy. Antihistamines (H1-antagonists) are used in mild reactions and glucocorticoids are given in order to prevent late phase reactions.

Adrenaline/epinephrine has been in use for more than 100 years. The consensus is that it is effective in treating anaphylaxis, even though—in the sense of evidence-based medicine—placebo controlled prospective studies are lacking. Such studies would not be ethically justifiable in any case (14, 26).

Mechanism of action of adrenaline/epinephrine

Adrenaline/epinephrine is one of three endogenous catecholamines, which is produced alongside noradrenaline in the adrenal glands and released in a scenario of stress, like cortisone. In combination with other blood pressure raising systems—for example, the renin-angiotensin system—this forms the basis for the spontaneous resolution of symptoms in many cases. Adrenaline binds to catecholamine receptors, but its specificity is dose-dependent: at low dosages, beta 1 and beta 2 receptor effects dominate, the effects mediated by alpha and beta receptors are balanced only at moderate dosages. At high dosages, vasoconstriction—mediated by alpha receptors—plays a greater part

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