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Anaphylaxis: Practice Essentials, Background, Pathophysiology. Ig. E- mediated anaphylaxis is the classic form of anaphylaxis, whereby a sensitizing antigen elicits an Ig. E antibody response in a susceptible individual. The antigen- specific Ig. E antibodies then bind to mast cells and basophils.

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Subsequent exposure to the sensitizing antigen causes cross- linking of cell- bound Ig. E, resulting in mast cell (and/or basophil) degranulation. Other types of immunologic anaphylaxis do not involve Ig. E. For example, anaphylaxis resulting from administration of blood products, including intravenous immunoglobulin, or animal antiserum is due, at least in part, to complement activation. Immune complexes formed in vivo or in vitro can activate the complement cascade.

Certain byproducts of the cascade—plasma- activated complement 3 (C3a), plasma- activated complement 4 (C4a), and plasma- activated complement 5 (C5a)—are called anaphylatoxins and can cause mast cell/basophil degranulation. When mast cells and basophils degranulate, whether by Ig. E- or non–Ig. E- mediated mechanisms, preformed histamine and newly generated leukotrienes, prostaglandins, and platelet- activating factor (PAF) are released. In the classic form, mediator release occurs when the antigen (allergen) binds to antigen- specific Ig. E attached to previously sensitized basophils and mast cells.

The mediators are released almost immediately when the antigen binds. Certain agents are thought to cause direct nonimmunologic release of mediators from mast cells, a process not mediated by Ig. E. These include opioids, dextrans, protamine, and vancomycin. Mechanisms underlying these reactions are poorly understood but may involve specific receptors (eg, opioids) or non–receptor- mediated mast cell activation (eg, hyperosmolarity). Inciting agents. The most common inciting agents in anaphylaxis are foods, Hymenoptera stings, and intravenous (IV) contrast materials. Anaphylaxis may also be idiopathic. Immunologic Ig. E- mediated reactions.

Typical examples of Ig. E- mediated anaphylaxis include the reactions to many foods, drugs, and insect stings. Hypersensitivity to foods is a problem encountered throughout the industrialized world. A study from Australia showed that more than 1. Ig. E- mediated food allergies. Reactions to foods are thought to be the most common prehospital (outpatient) cause of anaphylaxis. Certain foods are more likely than others to elicit an Ig.

E antibody response and lead to anaphylaxis. Foods likely to elicit an Ig. E antibody response in all age groups include peanuts, tree nuts, fish, and shellfish. Those likely to elicit an Ig. E antibody response in children also include cow’s milk, eggs, wheat, and soy. An analysis of 3. In placebo- controlled food challenges, peanut- sensitive patients can react to as little as 1.

A few years ago, egg- allergic individuals received influenza vaccination, but typically with a graded multi- dose protocol or based on skin prick testing to the vaccine itself. Given a dearth of recent evidence that egg- allergic individuals can safely receive the influenza vaccine with no increased risk of systemic reaction as compared to the general population, the most recent guidelines now recommend that all egg- allergic individuals should be vaccinated with a single dose of influenza vaccine. Furthermore, skin testing has no role because no evidence suggests this reliably identifies individuals at risk of a systemic reaction. Bacteria in spoiled fish produce enzymes capable of decarboxylating histidine to produce biogenic amines, including histamine and cis- urocanic acid, which is also capable of mast cell degranulation. Most cases of Ig.

E- mediated drug anaphylaxis in the United States are due to penicillin and other beta- lactam antibiotics. Approximately 1 in 5. Penicillin is metabolized to a major determinant, benzylpenicilloyl, and multiple minor determinants. Penicillin and its metabolites are haptens, small molecules that only elicit an immune response when conjugated with carrier proteins. Other beta- lactam antibiotics may cross- react with penicillins or may have unique structures that also act as haptens. Reactions to cephalosporins may occur in penicillin- allergic patients.

In these patients, older agents such as cephalothin, cephalexin, cefadroxil, and cephazolin are more likely to precipitate an allergic reaction than newer agents such as cefprozil, cefuroxime, ceftazidime, or ceftriaxone. This increased reactivity with the older agents is due to greater antigenic similarity of the side chain not present with the newer second- and third- generation agents. One report suggested that the actual incidence of anaphylaxis to cephalosporins in penicillin- anaphylactic patients is much lower than the 1. Only one patient (0. However, approximately 9.

Patients with less well- defined reactions to penicillin have a very low risk (1- 2%) of developing anaphylaxis to cephalosporins. The rate of skin- test reactivity to imipenem in patients with a known penicillin allergy is almost 5.

In contrast, no known in vitro or clinical cross- reactivity exists between penicillins and aztreonam. When either a penicillin or a cephalosporin is the drug of choice for a patient with a life- threatening emergency, a number of options exist. When the history is indefinite, the drug may be administered under close observation; however, when possible, obtain the patient’s informed consent.

Immediate treatment measures for anaphylaxis should be available. Alternatively, when the history is more convincing, an alternative agent should be chosen if it provides similar efficacy or one must pursue a desensitization protocol. Many other drugs have been implicated in Ig. E- mediated anaphylaxis, albeit less frequently. In the surgical setting, anaphylactic reactions are most often due to muscle relaxants but can also be due to hypnotics, antibiotics, opioids, colloids, and other agents.

The prevalence of latex allergy was higher during the 1. Manual Para Conquistar Mujeres Pdf Download. HIV and hepatitis B and C epidemics and the institution of universal precautions), but the incidence has decreased significantly since the widespread use of latex- free materials.

If latex is responsible for anaphylaxis in the perioperative setting, reactions tend to occur during maintenance anesthesia, whereas other agents tend to cause reactions during the induction of anesthesia. Volatile anesthetic agents can cause immune- mediated hepatic toxicity but have not been implicated in anaphylactic reactions. From 0. 5%- 3% of the US population experiences a systemic reaction after being stung. Local reaction and urticaria without other manifestations of anaphylaxis are much more common than full- blown anaphylaxis after Hymenoptera stings. Adults with generalized urticaria are at increased risk for anaphylaxis with future stings, but a local reaction, regardless of severity, is not a risk factor for anaphylaxis. Caution patients treated and released from the emergency department (ED) after an episode of anaphylaxis or generalized urticaria from Hymenoptera envenomation to avoid future exposure when possible.

Consider referral to an allergist for desensitization, particularly when further exposure is likely. Additionally, consider prescribing a treatment kit with an epinephrine autoinjector and oral antihistamine.

Both are effective measures in preventing or ameliorating future reactions. Allergen- specific subcutaneous immunotherapy (SCIT) can cause Ig. E- mediated anaphylaxis. Allergy injections are a common trigger for anaphylaxis. This is not unexpected, because the treatment is based on injecting an allergen to which the patient is sensitive. However, life- threatening reactions are rare.

Three studies suggest that fatalities from SCIT occur at a rate of approximately 1 death per 2,5. Of 6. 46 allergist- immunologists who responded to a survey on reactions, 2. NFRs. The investigators defined an NFR as respiratory compromise, hypotension, or both, requiring emergency epinephrine.