Anaphylaxis is an immune response caused when a person is exposed to an allergen for the second time. This is a type I, immunoglobulin E (IgE) mediated response. An anaphylactoid reaction is clinically indistinguishable to this but does not occur as the result of an immune response. Both conditions can produce life-threatening systemic changes that ultimately cause airway obstruction and circulatory collapse. Bronchial smooth muscle constricts causing bronchospasm, while vascular smooth muscle relaxes, and there is increased capillary permeability causing hypotension and potential shock. In both anaphylaxis and anaphylactoid reactions, the antigen stimulates release of histamine, prostaglandin, and leukotriene from basophils and mast cells. The way in which this occurs varies between the two processes. In anaphylaxis, the antigen initially stimulates production of IgE, which binds to the mast cells and basophils. When the antigen is reintroduced, it binds to the IgE already attached to the cells, resulting in an indirect release of chemical mediators from the cells. In an anaphylactoid reaction, this release is usually the result of a direct binding of the antigen to the cells, or of activation of the complement system. IgE is not involved. The end result of both processes is the same. Note that the term anaphylaxis will be used here to cover both types of reaction. Most reactions will occur within minutes of exposure to the allergen and usually within an hour. There may or may not be a previous history of anaphylaxis or allergy. Many allergens are commonly found, such as nuts, strawberries, and stings. From a prescribing viewpoint, it is imperative that you ascertain the allergy status of any players to whom you prescribe any medications. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or Voltarol and antibiotics such as the penicillin family are well known to have a side effect profile which includes allergy or anaphylaxis. In many of these cases, the player will be aware of the reaction they are having. It is the clinician’s responsibility to ensure an appropriate history is taken prior to prescribing these medications. Patients who suffer from asthma are recognized to experience more severe reactions and have a higher incidence of death from anaphylaxis, especially if there is a delay in administration of adrenaline. (Asthma should also be considered in the possible differential diagnosis of anaphylaxis.) The clinical signs are all related to the effects of the mediators on the end organs ( ▶ Table 3.1). Body system Clinical manifestation Airway Swelling of tongue or mucosal surfaces, e.g. lips; stridor, hoarseness Breathing Wheezing, increased respiratory rate; cyanosis is a late sign Circulation Tachycardia, hypotension, increased capillary refill time Skin Flushed, itchy, urticaria GI Diarrhea or vomiting Assessment and management is according to your ABCDE assessment, i.e., treating any immediate or emerging life-threatening features in order. It is also important to remove the allergen if at all possible (remove the sting with forceps, for example). The distinction between an allergy and anaphylaxis has been simplified such that anaphylaxis should be considered likely when all three of the criteria below are present: Rapid progression of symptoms. Skin or mucosal changes in association with either. Airway compromise and/or respiratory compromise and/or circulatory compromise (i.e., decreased blood pressure [BP]). Skin changes vary from erythema to urticaria (similar in appearance to the rash of a nettle sting). Angioedema is a skin manifestation similar to urticaria but involving deeper tissues such as submucosal or subcutaneous rather than the skin surfaces in urticaria. Skin changes are present in the vast majority of cases of anaphylaxis but may be absent in up to 20% of cases. In contrast, an allergy may occur with skin or mucosal changes, but without rapid progression or the associated A, B, or C system collapse. Remember, in approximately 20% of patients suffering an anaphylactic reaction, there may be no skin changes. Also, skin changes in isolation are not diagnostic of anaphylaxis and so the entire clinical picture needs to be considered. Diarrhea or vomiting may occur as part of the anaphylaxis reaction but neither is critical in terms of diagnosis. Many people believe themselves to be allergic to a medication when it is in fact a side effect rather than allergy. See http://www.resus.org.uk/pages/reaction.pdf for more information on anaphylaxis. This is summarized in the algorithm in ▶ Fig. 3.1. It is important to note that the system of assessment and treatment follows the ABCDE approach described earlier in Chapter ▶ 2. The immediate treatment will depend slightly on the experience of the clinician, the available equipment, and monitoring. It should be noted, however, that the algorithm clearly describes the initial treatment of the patient with adrenaline, chlorpheniramine, and hydrocortisone, all via the intramuscular (IM) route and therefore no intravenous (IV) cannula is actually required for treatment to commence. Fig. 3.1 Anaphylaxis algorithm. (Copyright European Resuscitation Council – www.erc.edu – 2016_NGL_043.) Oxygen should not be forgotten, as it is the first drug given. It should be applied using a trauma mask with a reservoir bag and a maximum flow rate—usually 15 L per minute. In anaphylaxis, lying the player down and elevating their legs is likely to be helpful only as a temporary measure. If this needs to be done, it indicates that the patient is likely to require IV fluids. The downside of someone lying down with their legs elevated is that if there are airway or breathing problems, they are far more likely to be trying to sit up to allow their body position to help with this. Adrenaline is given intramuscularly not intravenously. The dose administered IM is from 1:1,000 solution—0.5 mg in an adult = 0.5 mL IM 1:1,000. IV adrenaline only has a place in the treatment of an arrested player or a player under specialist care with full resuscitation equipment and monitoring. The dose is administered in the anterolateral aspect of the middle third of the thigh and can be re-administered after 5 minutes if there is no improvement in the player’s condition. Recent studies suggest it may be beneficial to use a blue or green needle in order to ensure the muscle is reached. Autoinjectors may be carried by some athletes. It is vital that you are familiar with the past medical history of each player in order to know who is taking what medication, when, and why. Autoinjectors are no different, and being aware of any previous problems with anaphylaxis is a very useful first stage in being prepared to deal with them. A dose via autoinjector is either 0.3 or 0.15 mg. Use of these medications is theoretical rather than evidence based. They should be administered after the primary survey and treatments have already started as they will not affect the immediate course of the illness (first few hours). Steroids may be beneficial in shortening the course of the illness and this is especially true in patients with a past history of asthma. These are difficult to predict and rebound may occur in anyone suffering from an anaphylactic reaction. Research would suggest hospital monitoring for at least 6 hours and possibly up to 24 hours in anyone who has previously suffered from a rebound reaction. Although not specifically the remit of the sports physician, anyone in your care who has suffered from an anaphylactic reaction should be referred for specialist assessment to identify any specific triggering allergens. This may involve communication with the individual’s general practitioner or directly with an immunologist. As with anaphylaxis, the incidence of asthma is documented to be on the rise in the general European population. Although it is a shared responsibility of the player and doctor to make sure the doctor is aware of any predisposing medical conditions the player may have, ASSUME this responsibility at the very start of your involvement with the team and make sure you are up to date with medical problems, ongoing injuries, and current medications. Asthma is characterized by the triad of the following: Bronchoconstriction. Increased mucous production. Mucosal swelling due to inflammation. Symptoms are classically coughing, wheezing, and breathlessness. Precipitants are many and varied: Upper or lower respiratory tract infections. Exercise. Drugs—in sport, nonsteroidal anti-inflammatory medications such as ibuprofen or Voltarol are commonly prescribed and also well known to trigger bronchospasm. Poor compliance with treatment. Stress. Smoking. No specific trigger may be identified in many cases. The main problem in treating the condition is in correctly identifying asthma as the diagnosis in the face of other differential diagnoses: Anaphylaxis. Pneumothorax. Pulmonary thromboembolism (PTE). Pulmonary edema—unlikely in sport but possible as part of altitude illness. Pneumonia. The condition is likely to present in one of two ways: Very acute onset related to someone who has “brittle” airways disease with sudden onset of symptoms and little in the way of warning. More gradual deterioration in a player in whom asthma is known or suspected but who has not responded to treatment and who suddenly deteriorates. Use the ABCDE (Airway, Breathing, Circulation, Disability, Extraction from the field of play) approach in the initial assessment (see ▶ Fig. 1.1). Depending on the severity of the attack, it may or may not be possible to take a history from the player. An inability to complete sentences is a strong marker of severity and should be taken seriously. A: Are they breathing? (If not, then call for immediate help and follow cardiac arrest guidelines.) Consider checking for intraoral or mucosal swelling that may suggest an allergy or anaphylaxis as a differential. B: Are there signs of any of the following? Cyanosis. Respiratory rate. Symmetry of chest movement. Accessory muscle use. Fatigue—anyone who appears fatigued or in whom the respiratory rate or respiratory effort is declining (without an overall associated improvement in their condition in all other ways) is likely to suffer an imminent respiratory arrest. Saturations—if available to you.
3.1.1 Pathophysiology
3.1.2 Common Allergens
3.1.3 Clinical Manifestations
3.1.4 Recognizing Anaphylaxis
3.1.5 Immediate Management of Anaphylaxis
Adrenaline
Chlorpheniramine and Hydrocortisone
3.1.6 Biphasic Reactions
3.1.7 Referral
3.2 Asthma
3.2.1 Assessment of Acute Asthma
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