The management of anaphylaxis involves several important steps. First and foremost, it is crucial to ensure proper airway management. Additionally, early administration of adrenaline is essential, preferably in the anterolateral aspect of the middle third of the thigh. Aggressive fluid resuscitation is also necessary. In severe cases, intubation may be required. However, it is important to note that the administration of chlorpheniramine and hydrocortisone should only be considered after early resuscitation has taken place.

Adrenaline is the most vital medication for treating anaphylactic reactions. It acts as an alpha-adrenergic receptor agonist, which helps reverse peripheral vasodilatation and reduce oedema. Furthermore, its beta-adrenergic effects aid in dilating the bronchial airways, increasing the force of myocardial contraction, and suppressing histamine and leukotriene release. Administering adrenaline as the first drug is crucial, and the intramuscular (IM) route is generally the most effective for most individuals.

The recommended doses of IM adrenaline for different age groups during anaphylaxis are as follows:

– Children under 6 years: 150 mcg (0.15 mL of 1:1000)
– Children aged 6-12 years: 300 mcg (0.3 mL of 1:1000)
– Children older than 12 years: 500 mcg (0.5 mL of 1:1000)
– Adults: 500 mcg (0.5 mL of 1:1000)

Corticosteroids can be beneficial in preventing or reducing prolonged reactions. According to the current APLS guidelines, the recommended doses of hydrocortisone for different age groups are as follows:

– Children under 6 months: 25 mg administered slowly via intramuscular (IM) or intravenous (IV) route.
– Children aged 6 months to 6 years: 50 mg administered slowly via IM or IV route.
– Children aged 6 to 12 years: 100 mg administered slowly via IM or IV route.
– Children over 12 years: 200 mg administered slowly via IM or IV route.
– Adults: 200 mg administered slowly via IM or IV route.

It is important to note that the most recent ALS guidelines do not recommend the routine use of corticosteroids for treating anaphylaxis in adults. However, the current APLS guidelines still advocate for the use of corticosteroids in children to manage anaphylaxis.

Hereditary angioedema is a condition caused by a lack of C1 esterase inhibitor, a protein that is part of the complement system. It is typically inherited in an autosomal dominant manner. Symptoms usually start in childhood and continue sporadically into adulthood. Attacks can be triggered by minor surgical procedures, dental work, and stress. The main clinical signs of hereditary angioedema include swelling of the skin and mucous membranes, with the face, tongue, and extremities being the most commonly affected areas. There is often a tingling sensation before an attack, sometimes accompanied by a non-itchy rash.

Angioedema and anaphylaxis resulting from C1 esterase inhibitor deficiency do not respond to adrenaline, steroids, or antihistamines. Treatment requires the use of C1 esterase inhibitor concentrate or fresh frozen plasma, both of which contain C1 esterase inhibitor. In situations that may trigger an attack, short-term prophylaxis can be achieved by administering C1 esterase inhibitor or fresh frozen plasma infusions prior to the event. For long-term prevention, androgenic steroids like stanozolol or antifibrinolytic drugs such as tranexamic acid can be used.

Patients who are on beta-blockers may not respond effectively to adrenaline during anaphylaxis. Research conducted on animals and reported cases have indicated that glucagon can be utilized to counteract the effects of beta-blockade if initial adrenaline doses prove ineffective.

Although prednisolone and hydrocortisone can be beneficial later on, it typically takes 6-8 hours for them to take full effect. Therefore, they are unlikely to have any impact on the patient during the brief period it will take for the ambulance to arrive.

Anaphylaxis is a prime example of a type I hypersensitivity reaction. It is mediated by IgE antibodies. The complex formed by IgE and the antigen binds to Fc receptors found on the surface of mast cells. This binding triggers the degranulation of mast cells, leading to the release of histamine, proteoglycans, and serum proteases from their granules. It is important to note that anaphylaxis can only occur after prior exposure to the antigen. During the initial exposure, a sensitization reaction takes place, and it is only upon subsequent exposure to the antigen that anaphylaxis is triggered. The degranulation of mast cells is a result of a significant influx of calcium into these cells.

ACE inhibitors should not be used in individuals with HAE because they can enhance the effects of bradykinin. This can lead to drug-induced angioedema, which is a known side effect of ACE inhibitors. In individuals with HAE, ACE inhibitors can trigger attacks of angioedema.

Further Reading:

Angioedema and urticaria are related conditions that involve swelling in different layers of tissue. Angioedema refers to swelling in the deeper layers of tissue, such as the lips and eyelids, while urticaria, also known as hives, refers to swelling in the epidermal skin layers, resulting in raised red areas of skin with itching. These conditions often coexist and may have a common underlying cause.

Angioedema can be classified into allergic and non-allergic types. Allergic angioedema is the most common type and is usually triggered by an allergic reaction, such as to certain medications like penicillins and NSAIDs. Non-allergic angioedema has multiple subtypes and can be caused by factors such as certain medications, including ACE inhibitors, or underlying conditions like hereditary angioedema (HAE) or acquired angioedema.

HAE is an autosomal dominant disease characterized by a deficiency of C1 esterase inhibitor. It typically presents in childhood and can be inherited or acquired as a result of certain disorders like lymphoma or systemic lupus erythematosus. Acquired angioedema may have similar clinical features to HAE but is caused by acquired deficiencies of C1 esterase inhibitor due to autoimmune or lymphoproliferative disorders.

The management of urticaria and allergic angioedema focuses on ensuring the airway remains open and addressing any identifiable triggers. In mild cases without airway compromise, patients may be advised that symptoms will resolve without treatment. Non-sedating antihistamines can be used for up to 6 weeks to relieve symptoms. Severe cases of urticaria may require systemic corticosteroids in addition to antihistamines. In moderate to severe attacks of allergic angioedema, intramuscular epinephrine may be considered.

The management of HAE involves treating the underlying deficiency of C1 esterase inhibitor. This can be done through the administration of C1 esterase inhibitor, bradykinin receptor antagonists, or fresh frozen plasma transfusion, which contains C1 inhibitor.

In summary, angioedema and urticaria are related conditions involving swelling in different layers of tissue. They can coexist and may have a common underlying cause. Management involves addressing triggers, using antihistamines, and in severe cases, systemic corticosteroids or other specific treatments for HAE.

Anaphylaxis is a type I hypersensitivity reaction, where the body’s response is triggered by the attachment of an antigen to a specific antibody. This attachment then leads to the release of histamine and other mediators, such as leukotrienes, tumor necrosis factor, and various cytokines, from mast cells and basophils. These substances are released when these cells are exposed to the antigen.

Hereditary angioedema is a condition caused by a lack of C1 esterase inhibitor, a protein that is part of the complement system. It is typically inherited in an autosomal dominant manner. Symptoms usually start in childhood and continue sporadically into adulthood. Attacks can be triggered by minor surgical procedures, dental work, and stress. The main clinical signs of hereditary angioedema include swelling of the skin and mucous membranes, with the face, tongue, and extremities being the most commonly affected areas. There is often a tingling sensation before an attack, sometimes accompanied by a non-itchy rash.

Angioedema and anaphylaxis resulting from C1 esterase inhibitor deficiency do not respond to adrenaline, steroids, or antihistamines. Treatment requires the use of C1 esterase inhibitor concentrate or fresh frozen plasma, both of which contain C1 esterase inhibitor. In situations that may trigger an attack, short-term prophylaxis can be achieved by administering C1 esterase inhibitor or fresh frozen plasma infusions prior to the event. For long-term prevention, androgenic steroids like stanozolol or antifibrinolytic drugs such as tranexamic acid can be used.

The mast cell tryptase test, also known as the tryptase test, is a valuable tool for detecting mast cell activation and confirming the diagnosis of anaphylaxis in cases where there is uncertainty. Tryptase is the primary protein found in mast cells. During anaphylaxis, mast cells release their contents, leading to an increase in blood tryptase levels. Typically, these levels start to rise approximately 30 minutes after symptoms begin, reach their peak at 1-2 hours, and return to normal within 6-8 hours.

For optimal results, it is recommended to collect three timed samples. The first sample should be taken as soon as possible after resuscitation efforts have commenced. The second sample should be obtained 1-2 hours after the onset of symptoms. Lastly, a third sample should be collected at the 24-hour mark to establish a baseline level.

While skin allergy tests, like the patch test, and blood tests for specific IgE can help identify the trigger of an allergic reaction, they alone cannot confirm the occurrence of anaphylaxis. The mast cell tryptase test, on the other hand, provides valuable information in confirming the diagnosis.

In some cases, the signs of skin or mucosal involvement may be difficult to detect or may not be present at all. The Royal College of Emergency Medicine (RCEM) states that anaphylaxis is likely when three specific criteria are met: the illness has a sudden and rapid onset, there are noticeable changes in the skin or mucosal areas such as flushing, hives, or swelling, and there are severe problems with the airway, breathing, or circulation that pose a life-threatening risk.

Further Reading:

Anaphylaxis is a severe and life-threatening hypersensitivity reaction that can have sudden onset and progression. It is characterized by skin or mucosal changes and can lead to life-threatening airway, breathing, or circulatory problems. Anaphylaxis can be allergic or non-allergic in nature.

In allergic anaphylaxis, there is an immediate hypersensitivity reaction where an antigen stimulates the production of IgE antibodies. These antibodies bind to mast cells and basophils. Upon re-exposure to the antigen, the IgE-covered cells release histamine and other inflammatory mediators, causing smooth muscle contraction and vasodilation.

Non-allergic anaphylaxis occurs when mast cells degrade due to a non-immune mediator. The clinical outcome is the same as in allergic anaphylaxis.

The management of anaphylaxis is the same regardless of the cause. Adrenaline is the most important drug and should be administered as soon as possible. The recommended doses for adrenaline vary based on age. Other treatments include high flow oxygen and an IV fluid challenge. Corticosteroids and chlorpheniramine are no longer recommended, while non-sedating antihistamines may be considered as third-line treatment after initial stabilization of airway, breathing, and circulation.

Common causes of anaphylaxis include food (such as nuts, which is the most common cause in children), drugs, and venom (such as wasp stings). Sometimes it can be challenging to determine if a patient had a true episode of anaphylaxis. In such cases, serum tryptase levels may be measured, as they remain elevated for up to 12 hours following an acute episode of anaphylaxis.

The Resuscitation Council (UK) provides guidelines for the management of anaphylaxis, including a visual algorithm that outlines the recommended steps for treatment.
https://www.resus.org.uk/sites/default/files/2021-05/Emergency%20Treatment%20of%20Anaphylaxis%20May%202021_0.pdf