Anaphylaxis is an immunologically mediated, potentially life-threatening syndrome. It occurs when a hypersensitive reaction to a usually innocuous antigen causes an exaggerated response. A common and increasingly prevalent allergen is found in nuts. The current incidence of allergic reactions to nuts is approximately one in 80 (Tariq et al, 1996) and is increasing, particularly among children (Armstrong and Rylance, 1999).
VOL: 96, ISSUE: 42, PAGE NO: 41
Ben King, RGN, is a registered instructor in Advanced Life Support (ALS) and Advanced Paediatric Life Support (APLS), Gloucestershire Royal NHS Trust
Peanuts, which are actually a legume and not a nut, are the most likely to induce an anaphylactic response, followed by Brazil nuts and then almonds (Ewan, 1996). Anaphylactic and anaphylactoid responses can be either immunoglobulin E (IgE) or non-IgE mediated.
Anaphylactic reactions (IgE mediated)
The recognition of an antigen is part of the body’s immune response and two molecules are involved in this process: immunoglobulins and T-cell antigen receptors. Immunoglobulins (of which IgE is one) are glycoproteins present in the serum and tissue fluids of all mammals. IgE is responsible for allergic reactions.
Following exposure to a trigger substance, antigen-specific IgE antibodies are produced which then sensitise mast cells and basophils. When exposure to the antigen is repeated, these cells release histamine and other substances, such as the leukotrienes and prostaglandins, which stimulate an anaphylactic response (Fig 1). An IgE mediated response can vary from one incident to another. This makes it very difficult for health care staff to predict the severity of a future reaction.
Anaphylactoid reactions (non-IgE mediated)
Anaphylactoid reactions are treated identically to anaphylactic reactions and are caused by a mechanism that is still unclear. An anaphylactoid reaction occurs at the first exposure to a substance, for instance a contrast medium during radiographic procedures.
Guidelines for treatment
Since anaphylactic reactions are so severe, definitive trials are not possible. Despite this, the project team of the Resuscitation Council (UK) put forward guidelines in 1999 for the treatment and management of anaphylaxis (Figs 2 and 3). Those known to suffer anaphylactic responses will have emergency treatment available at home. Early treatment may prevent the onset of acute anaphylaxis which can cause circulatory collapse, bronchospasm and angio-oedema.
Early signs and symptoms
It is essential that all sufferers are aware of the symptoms of an anaphylactic reaction (Box 1). This is equally important for parents, teachers and carers of these individuals.
Shock can be defined as a state when there is inadequate perfusion to the major organs (Advanced Life Support Course Sub-Committee of the Resuscitation Council (UK), 1998). This can be caused by a number of factors such as a reduced circulating volume of plasma in the case of dehydration, or through haemorrhage. In the case of anaphylaxis, shock occurs as a result of distributive shock caused by plasma leaking out of the circulating bloodstream and vasodilation of the vascular bed. The first steps in treatment are as follows:
- Resuscitation - if the casualty is unresponsive, is not breathing and has no pulse, start cardiopulmonary resuscitation, according to standard protocols for infants, children or adults. Specific measures for the management of cardiac arrest due to anaphylaxis are defined for adults in the guidelines of the Project Team of the Resuscitation Council (1999);
- Remove the allergen - it is very important to remove the allergen. If the allergen is being/has been eaten, it may not be possible to remove it. But if the symptoms occur as ingestion is taking place, it may well be possible to remove some of the substance from the person’s mouth and lips;
- Summon help - this is of great importance, and applies to situations inside and outside hospital;
- Positioning - the casualty should be positioned comfortably but lying flat, if their condition allows, with the feet elevated - although individuals with a threatened airway are unlikely to tolerate this. Do not force babies and children to comply with this as crying causes turbulence which will increase the difficulty in breathing and may lead to respiratory arrest.
The aim of drug treatment is to counteract bronchospasm, peripheral vasodilation, capillary leakage, poor tissue perfusion and further histamine release.
- Oxygen therapy - this involves the delivery of 100% oxygen at 15L per minute via a face mask with a reservoir bag. The aim is to minimise the potential of hypoxaemia and to counteract the loss of oxygen which occurs as a result of increased expenditure of energy and oxygen due to a compromised airway. Children have a higher oxygen requirement per kilogram of body weight and lower oxygen reserves than adults due to their increased metabolic rate. This means that their oxygen is used more quickly;
- Adrenaline - adrenaline has both alpha and beta-agonist effects. Alpha-agonists stimulate alpha receptors and beta-agonists stimulate beta receptors. Alpha-receptor stimulation leads to vasoconstriction. Beta-1 receptor stimulation leads to increased heart rate and an increased pumping action; Beta-2 receptor stimulation leads to dilation of peripheral and coronary arteries;
The alpha effect causes peripheral vasoconstriction which preserves circulation to the heart and brain. Conversely, adrenaline causes vasodilation in the vessels of these two vital organs. The beta effect is to relieve bronchospasm and laryngeal oedema which assists with the work of breathing and oxygen delivery.
The Project Team of the Resuscitation Council (UK) recommends that adrenaline is administered intramuscularly for all patients with a spontaneous circulation, where the heart is still beating and pumping blood around the body and who present with the following symptoms:
- Clinical signs of shock (increased heart rate, increased breathing, shallow breathing, pallor, cool peripheries, altered level of consciousness, such as heightened anxiety, drowsiness or unconsciousness);
- Airway swelling;
- Breathing difficulties, such as wheezing or stridor.
Known sufferers may self-administer an adrenaline injection. This can be done quickly and simply via specially designed, preloaded syringes. Some of these devices deliver the dose with enough pressure to penetrate through the rubber bung protecting the needle, through clothing and into the muscle, to ensure that it can be delivered at the first signs of an anaphylactic reaction. It also eliminates the need for undressing or gaining access to bare skin.
- Intravenous fluids - crystalloid or colloid solutions should be administered as quickly as possible following the onset of an anaphylactic response to improve perfusion of oxygen and therefore aid in its delivery.
Additional drugs used in anaphylaxis
- Antihistamine (H1 receptor agonist) - this is not a first-line intervention because by the time symptoms develop, histamine has already been released into the circulation. However, antihistamine will prevent further release so that the episode may be less severe and last a shorter time. For severe cases it should be given with caution as intravenous or intramuscular administration may induce hypotension;
- Hydrocortisone - as with antihistamines, hydrocortisone is not a management priority, but if given early it is likely to assist in reducing the length and severity of the anaphylactic episode. This is particularly important in patients who have a pre-existing condition such as asthma;
- Bronchodilators - inhaled beta-2 agonists, such as salbutamol, can be used to treat symptoms relating to bronchospasm when symptoms of a compromised airway persist. The nebuliser should be driven by oxygen in all children;
- Glucagon - patients on beta-blockers may not respond to emergency doses of adrenaline in the usual way, due to their systemic action. These patients should be given glucagon to counteract this problem. Glucagon produces chronotropic (makes the heart beat faster) and inotropic (makes the heart beat stronger) effects in these patients and thus improves cerebral and system haemodynamics which reverse the signs of shock.
After an episode
In many instances the effect of the allergen is immediate, and so it can easily be identified. However, in other cases the cause may not be obvious and further investigation is needed.
A test for mast-cell tryptase should be taken within the first hour of an attack and then repeated at two, 12 and 24 hours. It shows the level of tryptase released from the mast cells as a result of anaphylactic and anaphylactoid reactions. It is an indicator of mast-cell activation, although it gives no clues as to the cause of the reaction.
A radio-allergosorbent test (RAST test) enables the laboratory to measure IgE antibodies which occur at very low levels in serum. The validity of this test is questionable as it can produce false positive and false negative results. The only sure way of determining what the patient will react to is through exposure to the substance.
Skin-prick testing and food challenges
Exposure to the suspected allergen is done firstly through a skin-prick test and then by ingestion. This sort of test may induce an anaphylactic response and so should be undertaken only by a specialist who has immediate access to the appropriate emergency facilities. In addition, there must be someone present who is trained in advanced life-support techniques. The patient must always be cannulated before ingesting any potential allergens, even in this controlled environment.
Research is being carried out to determine the different mechanisms of anaphylaxis and to develop methods of preventing it. It is hoped that a way to desensitise peanut allergy sufferers may be found by isolating the specific proteins in the plant that cause the reaction. Genetically modifying peanuts is also thought by some to be a potential answer if this protein can be isolated and either removed or made safe. Nevertheless, effective emergency management, alongside support and prevention of exposure to allergens, will remain of paramount importance for the foreseeable future.
Action Against Allergy, PO Box 278, Twickenham TW1 4QQ. Tel: 020 8892 2711.
The Anaphylaxis Campaign, PO Box 149, Fleet, Hampshire GU13 0FA. Tel: 01252 542029.
British Allergy Foundation, 30 Bellgrove Road, Welling, Kent DA16 3PY. Tel: 020 8303 8525.
The Resuscitation Council (UK), 5th Floor Tavistock House North, Tavistock Square, London WC1H 9HR. Tel: 020 7388 4678.