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Bùi Văn Quân đang tìm kiếm từ khóa After initial identification of potential for anaphylaxis, the nurses priority assessment is được Update vào lúc : 2022-09-03 07:06:03 . Với phương châm chia sẻ Thủ Thuật về trong nội dung bài viết một cách Chi Tiết Mới Nhất. Nếu sau khi tham khảo tài liệu vẫn ko hiểu thì hoàn toàn có thể lại phản hồi ở cuối bài để Ad lý giải và hướng dẫn lại nha.

Anaphylaxis is defined as “a serious, generalized or systemic, allergic or hypersensitivity reaction that can be life-threatening or fatal” by the International consensus on (ICON) anaphylaxis (Simons et al., 2014).

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    AnaphylaxisAnaphylaxisAnaphylaxisPrevention of Anaphylaxis in Specific SettingsAnaphylaxisIntroduction and BackgroundAnaphylaxis1 Define anaphylaxis.2 Define anaphylactoid reaction.3 What are the most common causes?4 What are the most common “target” organs?5 What are the most common signs and symptoms?6 What is the role of diagnostic studies?7 What is the differential diagnosis?8 What is the most common form of anaphylaxis? How is it treated?9 What is the best route for epinephrine administration?10 Describe the initial treatment for life-threatening forms of anaphylaxis.11 What are the adjuncts to initial epinephrine and airway management?12 What is unique about the treatment of anaphylaxis in patients who are taking beta blockers?13 What are the complications of bolus IV epinephrine administration?14 Is there a role for prophylactic treatment in anaphylaxis? How is this performed?15 Describe the out-of-Hospital treatment of anaphylaxis.AnaphylaxisAnaphylaxisPATHOPHYSIOLOGYAnaphylaxisEpidemiologyAnaphylaxisUrticaria, Angioedema, and AnaphylaxisEtiology of AnaphylaxisHow do you assess for anaphylaxis?What actions should the nurse take when caring for a client with an anaphylactic reaction?How do nurses treat anaphylaxis?Which of the following represent initial signs and symptoms of a patient in respiratory distress?

From: Encyclopedia of Infection and Immunity, 2022

Anaphylaxis

Paul J. Turner, in Reference Module in Biomedical Sciences, 2022

Abstract

Anaphylaxis is a serious systemic hypersensitivity reaction that is usually rapid in onset and may cause death. Severe anaphylaxis is characterized by potentially life-threatening compromise in airway, breathing and/or the circulation. The incidence of anaphylaxis is probably increasing but fatal anaphylaxis remains rare. Medications appear to be the most common cause of anaphylaxis admissions and fatalities, with different triggers associated with specific clinical presentations which are not solely attributable to the route of exposure. While the majority of anaphylaxis reactions are meditated through the IgE receptor, it is likely that other mechanisms exist, particularly with respect to drug-induced reactions. Irrespective of pathophysiology, the first line treatment of anaphylaxis is the administration of intramuscular adrenaline (epinephrine) which can be repeated after 5–10 min. Refractory anaphylaxis, characterized by a suboptimal response to 2 appropriate doses of intramuscular adrenaline, is a critical life-threatening condition which will often respond to aggressive fluid therapy in conjunction with an intravenous adrenaline infusion. Following anaphylaxis to a previously unidentified allergen, individuals should ideally be referred for specialist assessment and evaluation of modifiable risk factors. Those risk of further accidental exposure in the community (e.g., venom stings, food allergens) should be prescribed an adrenaline auto-injector device, and receive adequate training in its use.

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Anaphylaxis

Simon G.A. Brown, Paul J. Turner, in Middleton's Allergy Essentials, 2022

Abstract

Anaphylaxis is a severe, immediate-type generalized hypersensitivity reaction affecting multiple organ systems and characterized its most severe by bronchospasm, upper airway angioedema, hypotension and collapse. Lifetime prevalence is estimated to be 0.05–2%, but while anaphylaxis can be life-threatening, fatal anaphylaxis is rare. Drugs, foods and insect stings are the commonest triggers. The cornerstones of emergency management are support of the airway and/or ventilation, a supine position, epinephrine, and volume expansion. In the community setting, early administration of rescue epinephrine and contact with Emergency Services are of equal importance. Following an episode of anaphylaxis, prevention of further episodes requires identification of likely trigger(s) and co-factors, optimizing the management of comorbidities, allergen avoidance strategies, and immunotherapy if available. Patient education including an Anaphylaxis Action Plan and an epinephrine auto-injector should be considered where an allergen may be encountered unexpectedly (food and insect sting anaphylaxis, idiopathic anaphylaxis).

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Anaphylaxis

F. Estelle R. Simons, in Pediatric Allergy: Principles and Practice (Third Edition), 2022

Prevention of Anaphylaxis in Specific Settings

Unique aspects of anaphylaxis prevention in the physician's office or clinic setting and in school settings will be reviewed briefly.

Physician's Office or Clinic

Anaphylaxis in this setting, although probably inevitable, is not a random sự kiện. It can be triggered by a food or drug challenge test, infusion of a biologic agent, subcutaneous allergen-specific immunotherapy and, rarely, by allergen skin tests or vaccinations to prevent infectious diseases. In this setting, the allergen and time of exposure are known and the healthcare professionals involved are likely aware of the patient's co-morbidities, concurrent medications and body toàn thân mass (weight).1

Prevention of anaphylaxis in an office or clinic setting involves awareness of procedure-related risk factors and patient-related risk factors, careful selection of patients for diagnostic and therapeutic interventions, reassessment of patients before each intervention and deferral of interventions when clinically indicated, for example in a patient with an asthma exacerbation or an FEV1 of ≤ 70% predicted.1

Specific wait times after diagnostic and therapeutic interventions are suggested to ensure patient safety; for example, 30 minutes after allergen immunotherapy, one hour after completion of a food challenge and 30 minutes to 2 hours after omalizumab injections for asthma. As patients and caregivers can be inconvenienced by waiting, and sometimes try to leave early, an EAI should be prescribed and they should be trained to recognize anaphylaxis symptoms and use the EAI promptly if symptoms occur after they leave the office or clinic.50,67,68

Anaphylaxis in Schools and Other Community Settings

Twenty percent of children experience their first anaphylaxis episode school. The first episode can be fatal. Increased availability of stock (unassigned) EAIs that are not prescribed for a specific child but available for use in any child with anaphylaxis is anticipated to reduce morbidity and mortality in this setting. Prevention of anaphylaxis recurrences in schools, and preparedness to recognize and treat it, involves the student, the family, the student's physician and the school145–148 (Box 58-7).

In community settings, broader training in prompt recognition and treatment of anaphylaxis is needed not only for teachers and all other school personnel, but also for coaches, camp directors, childcare providers, restaurant and food industry workers, airline personnel and the public. The goal of training is to increase awareness that anaphylaxis is not a trivial lifestyle problem but rather a killer allergy that needs to be recognized and treated promptly. Increased availability of stock EAIs in public places such as shopping malls and sports facilities will contribute to decreased morbidity and mortality from anaphylaxis in community settings.1,2,144–150

Anaphylaxis education for everyone involved with infants, children and teens should emphasize the sudden onset and potentially rapid progression to multisystem involvement and life-threatening symptoms during an anaphylactic episode, the need to be prepared, to recognize and treat it promptly, and to understand the critical role of allergen avoidance in prevention of anaphylaxis recurrences.1,2,144–150

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Anaphylaxis

Suzanne M. Beno MD, in Pediatric Emergency Medicine, 2008

Introduction and Background

Anaphylaxis has long been recognized as a severe, life-threatening reaction that involves multiple target organs, including skin, respiratory, gastrointestinal, cardiovascular, and neurologic systems.1 Consensus regarding its exact definition currently does not exist and there is considerable disagreement about its prevalence, diagnosis, and management. A recent practice parameter addresses these issues and attempts to provide an evidence-based approach to the definition of this condition.2 Anaphylaxis is considered to be highly likely when any one of the following three criteria is present:

1

Acute onset of an illness (minutes to hours) involving skin/mucosa and either respiratory compromise or hypotension (associated symptoms)

2

Two or more of the following that occur rapidly after exposure (minutes to hours) to a likely allergen for that patient: skin/mucosal involvement, respiratory compromise, hypotension and associated symptoms, and persistent gastrointestinal symptoms

3

Hypotension after exposure to known allergen for that patient (minutes to hours)

The term anaphylaxis encompasses both immunoglobulin E (IgE)-mediated reactions and non-IgE-mediated mechanisms (anaphylactoid reactions); the difference impacts allergen counseling but is of little consequence in the immediate management of the patient.2

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Anaphylaxis

Vincent J. Markovchick MD, in Critical Care Secrets (Fourth Edition), 2007

1 Define anaphylaxis.

Anaphylaxis is a potentially life-threatening systemic immediate hypersensitivity reaction of multiple organ systems to an antigen-induced, immunoglobulin E–mediated immunologic mediator release in previously sensitized persons.

2 Define anaphylactoid reaction.

This is a potentially fatal syndrome that is clinically similar to anaphylaxis but is not an immunoglobulin E–mediated response. It may occur after a single first-time exposure to certain agents, such as radiopaque contrast truyền thông.

3 What are the most common causes?

Ingestion, inhalation, or parenteral injection of antigens that sensitize predisposed persons. Common antigens include drugs (e.g., penicillin), foods (e.g., shellfish, nuts, eggwhites), insect stings (e.g., hymenoptera) and animal bites (e.g., snakes), diagnostic agents (e.g., ionic contrast truyền thông), and physical and environmental agents (e.g., latex, exercise, cold). Idiopathic anaphylaxis is a diagnosis of exclusion that is made when no identifiable cause can be determined.

Volcheck GW, Li JT: Exercise-induced urticaria and anaphylaxis. Mayo Clin Proc 72:140–147, 1997.

4 What are the most common “target” organs?

The most common organ systems involved are the skin (e.g., urticaria, angioedema), mucous membranes (e.g., edema), upper respiratory tract (e.g., edema, hypersecretions), lower respiratory tract (e.g., bronchoconstriction), and cardiovascular system (e.g., vasodilatation, cardiovascular collapse).

5 What are the most common signs and symptoms?

The clinical presentation ranges from mild to life-threatening. Mild manifestations, which occur in most people, include urticaria and angioedema. Life-threatening manifestations involve the respiratory and cardiovascular systems. Respiratory signs and symptoms include acute upper airway obstruction presenting with stridor or lower airway manifestations of bronchospasm with diffuse wheezing. Cardiovascular collapse presents in the form of syncope, hypotension, tachycardia, and arrhythmias.

6 What is the role of diagnostic studies?

There is no role for diagnostic studies in anaphylaxis because diagnosis and treatment are based solely on clinical signs and symptoms. There is a role for skin testing either before administration of an antigen or in follow-up referral to determine the exact allergens involved. If the diagnosis is in doubt, additional studies may be indicated.

7 What is the differential diagnosis?

Anaphylaxis may be confused with septic and cardiogenic shock, asthma, croup and epiglottitis, vasovagal syncope, hereditary angioedema, carcinoid syndrome, hysterical stridor, myocardial infarction, or any acute cardiovascular or respiratory collapse of unclear etiology.

8 What is the most common form of anaphylaxis? How is it treated?

Urticaria, either simple or confluent, is the most benign and, fortunately, the most common clinical manifestation. This is thought to be due to a capillary leak mediated by histamine release. It may be treated by the administration of antihistamines (orally, intramuscularly, or intravenously) or epinephrine (intramuscularly). H1 blockers (e.g., diphenhydramine) should be used in all cases, and H2 blockers (e.g., cimetidine or ranitidine) should be added in refractory cases.

Runge JW, Martinez JC, Cavavuti EM: Histamine antagonists in the treatment of acute allergic reactions. Ann Emerg Med 21:237–242, 1992.

9 What is the best route for epinephrine administration?

Because the vast majority of patients do not require IV epinephrine, the ideal route for parental administration is intramuscular (IM) rather than subcutaneous. Recent studies have demonstrated that higher and more rapid peak plasma levels are achieved via the IM route.

Simons FER, Gu X, Simms KJ: Epinephrine absorption in adults: Intramuscular versus subcutaneous injection. J Allergy Clin Immunol 109:871–873, 2001.

10 Describe the initial treatment for life-threatening forms of anaphylaxis.

1

Upper airway obstruction with stridor and edema should be treated with high-flow nebulized oxygen, racemic epinephrine, and IV epinephrine. If airway obstruction is severe or increases, bag-valve-mask–assisted ventilation, endotracheal intubation, or cricothyroidotomy should be performed.

2

Acute bronchospasm should be treated with epinephrine. Mild to moderate wheezing in patients with a normal blood pressure may be treated with 0.01 mg/kg of 1:1000 epinephrine administered intramuscularly. If the patient is in severe respiratory distress or has a “quiet” chest, IV epinephrine should be administered via a drip infusion: 1 mg epinephrine in 250 mL D5W an initial rate of 1μg/min with titration to desired effect. Bronchospasm refractory to epinephrine may respond to a nebulized beta agonist, such as albuterol sulfate or metaproterenol, in recommended doses.

3

Cardiovascular collapse presenting with hypotension should be treated with a constant infusion of epinephrine, titrating the rate to attain a systolic blood pressure of 100 mmHg or a mean arterial pressure of 80 mmHg.

4

For patients in full cardiac arrest, administer 0.1–0.2 mg/kg of 1:10,000 epinephrine via slow IV push or via endotracheal tube. In addition, immediate endotracheal intubation or cricothyroid ostomy should be performed.

11 What are the adjuncts to initial epinephrine and airway management?

If intubation is unsuccessful and cricothyroid ostomy is contraindicated, percutaneous transtracheal jet ventilation via needle cricothyroid ostomy should be considered, especially in small children. Intravenous (IV) diphenhydramine, an H1 blocker (2 mg/kg), should be administered to all patients. Simultaneous administration of an H2 blocker such as cimetidine (300 mg IV or ranitidine 50 mg IV) should also be administered. Aerosolized bronchodilators such as metaproterenol are useful if bronchospasm is present. Corticosteroids are usually given but do not have an immediate positive effect. For refractory hypotension, pressors such as norepinephrine or dopamine can be administered. Corticosteroids have limited benefit because of their delayed onset of action, but they may be beneficial in patients with prolonged bronchospasm or hypotension.

12 What is unique about the treatment of anaphylaxis in patients who are taking beta blockers?

Patients who are taking beta blockers may not respond to epinephrine and antihistamines. Glucagon, which has positive inotropic and chronotropic effects mediated independently of α and β receptors, may be efficacious. Glucagon, 1 mg IV, should be administered, followed by 1–5 mg/h if necessary.

Javeed N, Javeed H, Javeed S, et al: Refractory anaphylactoid shock potentiated by beta-blockers. Cathet Cardiovasc Diag 39:383–384, 1996.

13 What are the complications of bolus IV epinephrine administration?

When epinephrine 1:10,000 is administered via IV push in patients who have an obtainable blood pressure or pulse, there is significant potential for overtreatment and the potentiation of hypertension, tachycardia, ischemic chest pain, acute myocardial infarction, and ventricular arrhythmias. Extreme care must be exercised in elderly patients and in those with underlying coronary artery disease. It is much safer to administer IV epinephrine by a controlled titratable drip infusion with continuous monitoring of cardiac rhythm and blood pressure.

Key Points: Anaphylaxis

1

Life-threatening “target organs” in anaphylaxis include upper airway mucosa (stridor), bronchial smooth muscle (bronchospasm), and the cardiovascular system (shock).

2

The IM route is preferred over the subcutaneous route for epinephrine administration in anaphylaxis.

3

IV epinephrine is indicated in severe respiratory distress and hypotension.

4

If the patient's condition is not responding to antihistamines and epinephrine, consider administering glucagon.

5

Except in cardiac arrest, IV epinephrine should be administered carefully via IV drip infusion to minimize the risk of severe sympathomimetic response effects.

14 Is there a role for prophylactic treatment in anaphylaxis? How is this performed?

When the potential benefits of treatment or diagnosis outweigh the risks (e.g., administration of IV contrast or animal bite antivenom), informed consent should be obtained if the patient is competent. Pretreatment with IV diphenhydramine (Benadryl) and corticosteroids should be carried out. An IV epinephrine infusion should be prepared. The patient should be in an intensive care unit setting with continuous monitoring of blood pressure, cardiac rhythm, and oxygen saturation. Full intubation and cricothyreotomy equipment should be the bedside. Administration of the antigen (e.g., rattlesnake antivenom) should be started very slowly with a physician the bedside who is capable of immediately administering IV epinephrine and managing the airway. Nonionic or low-osmolality contrast medium for diagnostic imaging studies should be administered to patients with a history of anaphylaxis to ionic contrast material.

15 Describe the out-of-Hospital treatment of anaphylaxis.

Patients who are known to be high risk (e.g., previous anaphylactic reaction to hymenoptera) should be prescribed and educated in the self-administration of epinephrine with an autoinjector the first sign of anaphylactic symptoms. In addition, self-administration of oral diphenhydramine is indicated for the treatment of mild reactions such as urticaria or concomitant with the administration of epinephrine.

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Anaphylaxis

Marion R. Sills MD, MPH, in Berman's Pediatric Decision Making (Fifth Edition), 2011

Anaphylaxis is an acute, potentially life-threatening allergic reaction with varied mechanisms and clinical presentations. Depending on the route of exposure to the inciting agent, symptoms can begin in minutes to hours; reactions within 3 hours of exposure are usually more severe.

A1. and B1.

On brief, initial history and physical examination, assess for the following clinical criteria for diagnosing anaphylaxis, which must include one of the following three criteria:

1.

Acute onset of illness involving skin/mucosal urticaria, pruritus, or swelling AND least one of the following:

a.

Respiratory compromise

b.

Hypotension/hypoperfusion

2.

Two or more of the following occurring rapidly after exposure to a likely allergen for that patient:

a.

Skin/mucosal urticaria, pruritus, or swelling

b.

Respiratory compromise

c.

Hypotension/hypoperfusion

d.

Persistent gastrointestinal symptoms.

3.

Hypotension/hypoperfusion after exposure to a known allergen for that patient

A2.

When necessary, stabilize the child before obtaining a history. When appropriate, attempt to determine the offending agent and the onset and progression of symptoms. Assess upper airway involvement by asking about pruritus or swelling of lips and tongue, throat tightness, stridor, dysphonia, or dysphagia; lower respiratory tract symptoms by cough, wheezing, dyspnea, or sense of chest tightness; cardiovascular abnormalities by tachycardia, syncope, or dizziness; central nervous system abnormalities by dizziness, syncope, altered mental status, or seizures; gastrointestinal symptoms of nausea, vomiting, abdominal cramps, and diarrhea; and cutaneous symptoms of hives (urticaria) or angioedema of the face or extremities. Note any prior history of atopy, including anaphylaxis, asthma, and eczema or hives. Note any associated chronic conditions, acute illnesses, and medications.

B2.

Initially, assess and stabilize airway, breathing, circulation, and level of consciousness before a more detailed physical examination. Assess the upper and lower airway, looking for swelling of lips or tongue, stridor, dysphonia, hypoxia, cough, tachypnea, wheezing, retractions, and poor aeration. Evaluate the cardiovascular system for tachycardia, decreased peripheral perfusion, arrhythmias, and hypotension. Central nervous system signs include altered mental status and seizure activity; either may indicate hypoxia or hypoperfusion.

B3.

After first assessing and stabilizing airway, breathing, circulation, and level of consciousness, a more complete physical examination should include examination of the skin for urticaria or angioedema and the gastrointestinal system for abdominal tenderness.

C1.

If this primary survey shows any compromise, immediately begin epinephrine, oxygen, and volume replacement. Epinephrine can be given intramuscularly (preferred) or subcutaneously, every 5 minutes to control hypotension and airway edema. Although not evidence based, nebulized, sublingual, intraosseous, and endotracheal routes can also be considered. Administer oxygen to patients with evidence of airway involvement, or who require multiple doses of epinephrine or other β agonists.

C2.

Patients with upper airway compromise require immediate airway management. Consider early intubation in patients with rapid onset of symptoms, prior anaphylaxis, and upper airway swelling, because airway edema can progress rapidly, making intubation increasingly difficult. Stridor, hypoxia, and respiratory distress are all late signs of upper airway compromise. If intubation is unsuccessful, consider attempting a cricothyrotomy. Although it has not been specifically studied in this context, some authors recommend concomitant nebulized epinephrine.

C3.

Because plasma volume may decline suddenly by 50% in anaphylaxis syndrome, give poorly perfused patients aggressive fluid resuscitation, starting with a rapid saline fluid bolus of 20 ml/kg, repeated as necessary. Patients should be placed in the recumbent position with legs elevated, unless precluded by dyspnea or vomiting. If shock persists, consider a continuous infusion of epinephrine (0.1 μg/kg/min, titrated up to 1.0 μg/kg/min). For patients with persistent hypotension, start vasopressors (see Shock, p. 32).

C4.

If response to volume replacement is inadequate, consider administering epinephrine intravenously, either through repeated dosing or via an infusion. Note that intravenous administration of epinephrine increases the risk for arrhythmia, so it should be used only in patients with hypotension who have not responded successfully to intramuscular epinephrine and volume replacement. If response to crystalloid infusion is inadequate, also consider colloid infusion.

C5.

For bronchospasm refractory to epinephrine, treat with supplemental oxygen, as well as bronchodilators, such as albuterol and/or ipratropium, and corticosteroids. For patients taking beta-blocking agents, which may attenuate the response to treatment, consider glucagon administration.

C6.

Assess the organ systems involved, as well as the degree of severity and progression. The first-line therapies for anaphylaxis are epinephrine, oxygen, and volume replacement. Consider giving an H1-receptor antihistamine, such as diphenhydramine, and an H2-receptor antihistamine, such as cimetidine or ranitidine; these work synergistically with the epinephrine therapy, but are considered second-line therapy to epinephrine, and should never be used alone in the treatment of anaphylaxis. Corticosteroids do not take effect during initial resuscitative efforts; their early use can help reduce the incidence and severity of late-phase reactions (Table 1).

C7.

Patients with a history of mild symptoms that have resolved before arrival in the emergency department may be discharged home after a short observation period (2–4 hours). Observe patients with a significant history of atopy (asthma, allergic rhinitis) for 12 to 24 hours because they are increased risk for a late-phase reaction.

D1.

Hospitalize any patient with significant symptoms of laryngeal edema or hypotension. Consider intensive care unit admission for patients requiring more than one dose of epinephrine.

D2.

Before discharge, patients diagnosed with anaphylaxis should: (1) be prescribed a self-injectable epinephrine device (one for each location—school, home, child care, etc.) and instructed in its use; (2) receive information regarding avoidance of the precipitating allergen; and (3) be advised to follow up with their primary care provider and consider follow-up evaluation with an allergist.

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Anaphylaxis

Grace M. Cheng, in Comprehensive Pediatric Hospital Medicine, 2007

PATHOPHYSIOLOGY

Two forms of anaphylaxis are recognized but are clinically indistinguishable and managed identically: immunoglobulin E (IgE)-mediated anaphylaxis and anaphylactoid reactions. IgE-mediated anaphylaxis occurs when allergen-specific IgE antibodies bind to high-affinity mast cell and basophil IgE FcεR1 receptors and cross-link these receptors. Typical triggers of IgE-mediated anaphylaxis include foods, Hymenoptera stings, latex, and antibiotics.

Anaphylactoid reactions appear to be caused by direct release of mast cell and basophil chemical mediators. Examples of anaphylactoid triggers include blood product infusions, hyperosmolar radiocontrast dye, vancomycin, and opiates.

Regardless of the initial cause, the mast cells and basophils degranulate and release histamine and other biochemical mediators that cause a multisystem response. Histamine response is mediated through histamine receptors. Vasodilation, tachycardia, and bronchospasm result from H1 receptors; headache, increased vascular permeability, flushing, and hypotension develop from both H1 and H2 receptor responses. Cutaneous pruritus and nasal congestion may be mediated by both H1 and H3 receptor pathways.1 Of note, mast cells also release β-tryptase during anaphylaxis; thus, transiently elevated levels of serum β-tryptase are consistent with anaphylaxis.

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Anaphylaxis

Sarah Stetson, Paul D. Siegel, in xPharm: The Comprehensive Pharmacology Reference, 2007

Epidemiology

The incidence of anaphylactic reactions is estimated between 1 in 10,000 and 1 in 20,000 during preoperative periods Laxenairne et al (2001). However, the overall occurrence of anaphylaxis is probably underestimated 1.2% to 15% of the United States population Neugut et al (2001). It has been reported that anaphylactic shock constitutes 9.8% of drug-induced allergic reactions reporting to the emergency room (ER) Pastorello et al (1986). The overall incidence of anaphylaxis in the ER is estimated 0.4%, with 9% of these being severe and involving loss of consciousness. Severe cases were associated with exposure to food, drugs, and hair dye. The most common etiologic agents are foods, such as fresh fruits and vegetables, nonsteroidal anti-inflammatory agents, and beta-lactam antibiotics. Those experiencing anaphylactic reactions are mainly women and those with atopy Pastorello et al (1986), Pastorello et al (2001). Sheikh and Alves Sheikh and Alves (2001) found age, sex, geographical, and socioeconomic variations in the incidence of anaphylaxis in England.

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Anaphylaxis

Michael D. Katz PharmD, in Decision Making in Medicine (Third Edition), 2010

The common signs and symptoms of anaphylaxis include an aura, rhinitis, cough, pruritus, urticaria, laryngeal edema, generalized edema, decreased sensorium, shock, bronchospasm, GI cramps, and vomiting. Rarely, patients may develop heart failure, pulmonary edema, and DIC. Other conditions such as vasovagal reactions, hyperventilation, globus hystericus, and hereditary angioedema may mimic aspects of anaphylaxis and should be ruled out before initiating aggressive therapy.

A.

Anaphylaxis is associated with a variety of factors, including foods, drugs, insect bites and stings, latex, semen, and exercise. More than one third of cases have no identifiable cause. Drugs associated with anaphylaxis include β-lactam antibiotics, sulfonamides, anesthetics, chymopapain, protamine, dextran, vaccines, and iodinated radiocontrast truyền thông. In any patient with anaphylaxis, obtain a complete exposure history, including any previous reactions.

B.

Local reactions usually consist of redness, swelling, and pain the site of injection. Systemic signs and symptoms may develop rapidly. Measures to slow absorption of the antigen from the injection site, such as application of ice or use of a venous (not arterial) occluding tourniquet, may be useful in the field until the patient reaches medical attention.

C.

Base the initial management of anaphylaxis on support of airway, breathing, and circulation. Place all patients in the Trendelenburg position and give supplemental oxygen. In patients with cardiac or respiratory arrest or serious arrhythmias, initiate Basic and Advanced Cardiac Life Support measures.

D.

Epinephrine is the mainstay of therapy for anaphylaxis; no other drug has proved as effective. Epinephrine reverses the effects of the mediators of anaphylaxis and may reduce the further release of these mediators. In most adults, give 0.3–0.5 ml of 1:1000 solution by SC injection (in children, 0.01 ml/kg). However, if the patient is in shock, give epinephrine through a central vein or instill into the endotracheal tube. If the desired response is not achieved and no adverse effects occur, repeat epinephrine in 10 minutes. Monitor elderly patients, especially those with underlying cardiac disease, very closely.

E.

In patients with severe bronchospasm, epinephrine and inhaled β 2 agonists (e.g., albuterol) are the most effective treatment. There is no evidence that IV theophylline is effective in the treatment of acute, severe bronchospasm, and it may increase the risk of cardiac arrhythmias. Early administration of an IV corticosteroid should be considered because these agents have a delayed onset of action. Methylprednisolone IV dosages of 50–125 mg every 6 hours has been used. In less severe cases, oral prednisone may be appropriate.

F.

Antihistamines serve as second-line therapy when a prolonged course is expected. H1 blocking agents such as diphenhydramine or hydroxyzine may be especially useful in treating pruritus. In patients with a prolonged or refractory course, the addition of the H2 blockers, such as ranitidine 50 mg IV or 150 mg PO, may be helpful.

G.

Instruct all patients with anaphylaxis in ways to avoid future exposure to the inciting agent. The cause of the episode, if known, should be documented clearly in the patient's medical record, especially in drug-induced anaphylaxis. Because existing therapy with beta blockers or angiotensin-converting enzyme (ACE) inhibitors could worsen anaphylaxis, those agents should be discontinued, if possible.

H.

In some instances specific preventive therapy may be indicated. Consider patients with bee-sting allergy who cannot easily avoid future exposures for desensitization. In patients with frequently recurrent idiopathic anaphylaxis, prophylactic therapy with corticosteroids and antihistamines has proved effective. Autoinjectors containing epinephrine also may be used by the patient risk for another serious reaction.

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Urticaria, Angioedema, and Anaphylaxis

Clive E.H. Grattan, Elena Borzova, in Clinical Immunology (Fifth Edition), 2022

Etiology of Anaphylaxis

Anaphylaxis is most commonly caused by foods, drugs, general anesthetic agents, insect stings, and latex. Rare causes include vaccines, semen, and aeroallergen inhalation. Exercise can occasionally cause anaphylaxis either on its own (exercise-induced anaphylaxis) or after ingestion of a food to which the individual is presensitized (food- and exercise-induced anaphylaxis). Up to 20% of patients with systemic mastocytosis present with anaphylaxis during their lifetime.38 Anaphylaxis mostly occurs in reaction to hymenoptera stings, NSAIDs, and opioids and in the perioperative setting.39 Idiopathic anaphylaxis accounts for up to 60% of anaphylaxis cases in ambulatory adults and for 10% of cases in children.40 It is increasingly recognized that some anaphylactic cases are multifactorial. Cofactors are thought to lower the threshold for the induction of anaphylaxis and are implicated in about 30% of anaphylaxis cases in adults.41 The risk of severe anaphylaxis is increased in patients taking beta-blockers or ACEIs, or both.28

The most common routes of allergen exposure are oral and parenteral, although inhalation of allergens (e.g., fish or legume allergens after cooking, latex particles in health care settings) or percutaneous penetration after skin contact can induce anaphylaxis in highly sensitized patients.

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URL: https://www.sciencedirect.com/science/article/pii/B9780702068966000429

How do you assess for anaphylaxis?

To help confirm the diagnosis: You might be given a blood test to measure the amount of a certain enzyme (tryptase) that can be elevated up to three hours after anaphylaxis. You might be tested for allergies with skin tests or blood tests to help determine your trigger.

What actions should the nurse take when caring for a client with an anaphylactic reaction?

The nurse would want to call a rapid response, place the patient on oxygen, and prepare for the administration of Epinephrine. This drug is the first-line treatment for anaphylactic shock. It will increase the blood pressure, decrease swelling, and dilate the airway.

How do nurses treat anaphylaxis?

Medications used for a patient risk or under anaphylactic shock are: Epinephrine. Epinephrine is given for its vasoconstrictive reaction; for emergency situations, an immediate injection of 1:1, 000 aqueous solution, 0.1 to 0.5 ml, repeated every 5 to 20 minutes is given. Diphenhydramine.

Which of the following represent initial signs and symptoms of a patient in respiratory distress?

Signs of Respiratory Distress. Breathing rate. An increase in the number of breaths per minute may mean that a person is having trouble breathing or not getting enough oxygen.. Color changes. ... . Grunting. ... . Nose flaring. ... . Retractions. ... . Sweating. ... . Wheezing. ... . Body position.. Tải thêm tài liệu liên quan đến nội dung bài viết After initial identification of potential for anaphylaxis, the nurses priority assessment is

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