Anaphylaxis


Article Author:
Kevin McLendon


Article Editor:
Britni Sternard


Editors In Chief:
Chaddie Doerr


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Trevor Nezwek
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
11/14/2018 12:16:53 AM

Introduction

Anaphylaxis is a common medical emergency and a life-threatening acute hypersensitivity reaction. It can be defined as a rapidly-evolving, generalized, multi-system, allergic reaction. Without treatment, anaphylaxis is often fatal due to its rapid progression to respiratory collapse. Historically speaking, anaphylactic reactions were categorized as IgE-mediated responses, while anaphylactoid reactions were categorized as IgE-independent events. Recently, these terms have been consolidated to a single diagnosis of anaphylaxis. Regardless of causation, the resultant clinical state and treatment for each reaction are identical; therefore, this unified terminology is currently the accepted vernacular. [1],[2],[3]

Etiology

Common inciting sources may include exposure to certain medications, foods, or insect stings. Immunotherapy injections directed at improving overall allergic response can induce a hyper-acute reaction. Latex hypersensitivity is occurring in increased prevalence, and as with any hypersensitivity, anaphylaxis is an inherent risk. Occasionally the offending agent is not identified; these reactions are identified as idiopathic anaphylaxis. [4],[5],[6]

Epidemiology

It is estimated that the world population has a lifetime prevalence of 1% to 3%, though the prevalence is increasing. While reactions can occur in any age group, they are most commonly noted in the younger population and developed countries. Unfortunately, anaphylaxis is often misdiagnosed or not diagnosed at all. The consequences of missed or delayed diagnosis result in increased morbidity and mortality. [7],[8],[9]

Pathophysiology

Anaphylaxis is typically an IgE-mediated (type 1) hypersensitivity reaction that involves the release of numerous chemical mediators from degranulation of basophils and mast cells after re-exposure to a specific antigen. IgE crosslinking and resultant aggregation of high-affinity receptors induce rapid release of stored chemical mediators. These chemical mediators include histamine, tryptase, carboxypeptidase A, and proteoglycans. Via activation of mediary phospholipase A, cyclooxygenases, and lipoxygenases then form arachidonic acid metabolites including leukotrienes, prostaglandins, and platelet-activating factors.[10],[11] The inflammatory response is then mediated by TNF-alpha (tumor necrosis factor), both as a preformed and late-phase reactant. Detailed physiology of these chemical mediators is as follows:

  • Histamine increases vascular permeability and vasodilation leading to hypo-perfusion of tissues. The body responds to these changes by increasing heart rate and cardiac contraction.

  • Prostaglandin D functions as a bronchoconstrictor, with simultaneous cardiac and pulmonary vascular constriction. It also potentiates peripheral vasodilation thus contributing to the hypo-perfusion of vital organs.

  • Leukotrienes add to the bronchoconstriction, vascular permeability, and induce airway remodeling.

  • Platelet activation factor also acts as a bronchoconstrictor and increases vascular permeability.

  • TNF-alpha activates neutrophils (as part of stress response leukocytosis) and increases chemokine synthesis.

Histopathology

Rapid mast cell and basophil degranulation are attributed as the causation for the overactive immune response that culminates in the clinical picture of anaphylaxis.

History and Physical

Clinical presentation often begins as a mild allergic reaction. The primary symptoms depend on the mode of exposure to the causative antigen. While cutaneous flushing with pruritus and urticaria are common, they may not develop until after respiratory symptoms occur, which is common in oral exposures. Fullness or a "lump in the throat," persistent clearing of the throat or difficulty breathing are all concerning symptoms of anaphylaxis and should be treated aggressively. Other respiratory symptoms include hoarseness, wheezing, and stridor. If any of these symptoms are present, rapid treatment should be initiated with intramuscular epinephrine.

Anaphylaxis is most often a rapidly evolving presentation, usually within one hour of exposure. Roughly half of the anaphylactic-related fatalities occur within this first hour; therefore, the first hour after initial symptom onset is the most crucial for treatment. It is important to note that the more rapid the onset and progression of symptoms, the more severe the disease process. Morbidity and mortality are most often related to loss of airway and distributive shock. Early recognition and aggressive treatment greatly reduce the risk of adverse outcomes.

The first hour is not the only time of concern; however, as anaphylactic reactions can also present in a biphasic manner in up to 20% of cases. Even after successful management of the initial presenting symptoms, there can be a recurrence of symptoms peaking 8 to 11 hours after the initial reaction. While the biphasic response is only clinically significant in 4% to 5% of patients with diagnosed anaphylaxis, the potentially fatal second reaction should not be dismissed after treatment of initial reaction.

While a majority of the focus is placed on the above symptoms of respiratory, cutaneous, and hypotension, it is important to understand and evaluate for any other signs of end-organ damage from hypo-perfusion. This may include abdominal pain and cramps, vomiting, hypotonia, syncope, or incontinence. Gastrointestinal (GI) symptoms are present in 25% to 30% of patients. While the loss of airway control due to laryngeal edema is the primary concern, one must not fail to recognize anaphylaxis in the patient who does not endorse upper airway edema or respiratory complaints.

Evaluation

The diagnosis of anaphylaxis is a clinical diagnosis; thus, laboratory studies or other diagnostics are not necessary. Most anaphylactic deaths occur within the first hour after antigen exposure, rapid recognition and action are imperative. [2],[12],[13]

Consideration for anaphylaxis is appropriate in the presence of 2 or more involved systems, even in the absence of airway involvement or hypotension (see above). A consensus criterion has been constructed to improve the clinical recognition to prevent delayed treatment as this poses a great risk to patients.

Clinical Criteria for Anaphylaxis (1 of the following with onset inside minutes to hours)*

Unknown exposure to an antigen yet rapidly developing urticaria or other skin/mucosal layer symptoms associated with any one of the following:

  1. Respiratory symptoms (dyspnea, wheeze, stridor, hypoxemia, inability to maintain patency; persistent cough and/or throat clearing can be heralding symptom) 
  2. Hypotension (systolic less than 90 mm Hg or a decrease of greater than 30% from baseline)
  3. Signs or symptoms of end-organ dysfunction, for example, hypotonia, syncope, incontinence

Likely exposure to an antigen and symptoms involving any 2 of the following body systems:

  1. Integumentary symptoms: Skin or mucosal layer (rash, pruritus, erythema, hives, swelling of the face, lips, tongue, or uvula)
  2. Respiratory symptoms: Dyspnea, wheeze, stridor, hypoxemia, inability to maintain patency; persistent cough and/or throat clearing can be heralding symptom
  3. Hypotension: Systolic less than 90 mm Hg or a decrease of greater than 30% from baseline
  4. Gastrointestinal symptoms: Persistent painful cramps or vomiting

Known exposure to an antigen and hypotension (systolic less than 90 mm Hg or a decrease of greater than 30% from baseline)

*Note: It is not required to meet these criteria to treat, only to serve as a guide for diagnosis

Angioedema can also mimic these symptoms. A key differentiation between angioedema and anaphylaxis is urticaria, the oral symptoms and need for airway control can otherwise mimic each other. When in doubt, treat aggressively.

Laboratory testing is of little to no use, as there is no accurate testing for diagnosis or confirmation. Serum histamine is of no use due to transient elevation and late presentation. Serum tryptase can be considered for confirmation of an anaphylactic episode as it remains elevated for several hours, however, as a diagnostic modality, this has low sensitivity.

Treatment / Management

Triage

Triage any allergic reaction with urgency as they are at risk for rapid deterioration with the development of anaphylaxis, if not already anaphylactic.[14],[15],[16]

Airway

Airway management is paramount. Thoroughly examine the patient for airway patency or any indications of impending loss of airway. Perioral edema, stridor, and angioedema are very high risk, and obtaining a definitive airway is imperative. Delay may reduce the chances of successful intubation as continued swelling occurs, increasing the risk for a surgical airway.

Decontamination

After the airway is secured, decontamination of offending agent (if known) is the next priority to prevent continued exposure and clinical worsening. Remove any stingers, if present. Do not attempt gastric lavage in cases of ingestion as this may not be effective and delays treatment.

Epinephrine

Epinephrine is given through intramuscular injection and at a dose of 0.3 to 0.5 mL of 1:1,000 concentration of epinephrine. Pediatric dosing is 0.01 mg/kg or 0.15 mg intramuscularly (IM) (epinephrine injection for pediatric dosage). Intramuscular delivery has proven to be both more rapid delivery and produce better outcomes than subcutaneous or intravascular. Note if intravenous (IV) epinephrine is to be given, the concentration required is 1:10,000, see next paragraph. The thigh is preferred to the deltoid when possible. Repeat studies have shown that providers often wait too long before giving epinephrine, it is the treatment of choice and the rapid benefit much outweighs the risks of withholding treatment. While most patients require only a single dose, repeat doses may be given every 5 to 10 minutes as needed until symptoms improve.

  1. If patients require multiple doses, a continuous infusion of epinephrine may be considered, start an initial IV infusion of 0.1 mg of 1:10,000 given over 5 to 10 minutes. If more is required, begin infusion at 1 microgram per minute and titrate to effect. Stop IV infusion if arrhythmia or chest pain develops. The risk of cardiovascular complication is much greater for IV epinephrine. For beta-blocked patients, close blood pressure monitoring is suggested due to the risk of unopposed alpha-adrenergic effects from epinephrine.

IV Fluid Resuscitation

Anaphylaxis induces a distributive shock that typically is responsive to fluid resuscitation and the above epinephrine. One to 2 L or 10 to 20 mL/kg isotonic crystalloid bolus should be given for observed hypotension. Albumin or hypertonic solutions are not indicated.

Adjunctive Therapies

Often when anaphylaxis is diagnosed co-treatment is initiated with steroids, antihistamines, inhaled bronchodilators, and vasopressors. Glucagon can also be used if indicated. These agents can assist in refractory initial anaphylaxis or aid in the prevention of recurrence and biphasic reactions.

Corticosteroids

Corticosteroids are given for the reduction of length or biphasic response of anaphylaxis. There is minimal literature to support this use specifically in anaphylaxis, but it has been proven effective in reactive airway diseases. Therefore, use, dosages, and proposed mechanism of action mimic those of airway management protocols. 

Methylprednisolone (80 to 125 mg IV) or hydrocortisone (250 to 500 mg IV) are the accepted treatments during the acute phase, after which oral treatment of prednisone (40 to 60 mg daily or divided twice per day) is continued for 3 to 5 days. Again, if the source is unknown and/or there is a concern for a prolonged time prior to physician follow up steroid taper up to 2 weeks may be provided. Mineralocorticoid activity is responsible for fluid retention; in those at risk, dexamethasone and methylprednisolone are the preferred agents as they induce the least mineralocorticoid effect.

Antihistamines

Antihistamines are often routinely used; most commonly is H­blocker administration of diphenhydramine 25 to 50 mg IV/IM. While the clinical benefit is unproven in anaphylaxis, its utility is evident in more minor allergic processes. In severe cases, H blockers such as ranitidine (50 mg IV over 5 minutes) or cimetidine (300 mg IV) may also be used in conjunction H­blocker as there is evidence suggesting histamine has crossover selectivity of receptors. Note that cimetidine has multiple precautions in at-risk populations such as renal or hepatic impaired patients, or those taking beta-blockers. While IV is the initial route during stabilization, once the patient is stabilized they may be switched to oral if continued therapy is desired.

Bronchodilators

Bronchodilators are useful adjuncts in patients with bronchospasm. Patients with previous histories of respiratory disease, most notably asthma are at highest risk. Treated with inhaled beta-agonists are the first-line treatment in wheezing; albuterol alone or as ipratropium bromide/albuterol. If there is refractory wheezing IV magnesium is appropriate with dosage and treatment similar to severe asthma exacerbations.

Vasopressors

Vasopressors may be substituted when a patient requires more doses of epinephrine but has unacceptable side effects from the epinephrine IV infusion (arrhythmia or chest pain). In which case there has been no clear second line pressor identified, treatment guidelines would follow that of any other patient in hypotensive shock.

Glucagon

Glucagon is the reversal agent for beta-blockers and can be used as such if needed in cases where anaphylaxis is resistant to treatment in patients with beta-blockade. Known side effects include nausea, vomiting, hypokalemia, dizziness, and hyperglycemia.

Differential Diagnosis

A vasovagal episode, myocardial ischemia/infarction, arrhythmias, asthma, seizure, epiglottitis, angioedema, foreign body airway obstruction, mastocytosis, carcinoid syndrome, vocal cord dysfunction, anxiety, gastroenteritis, among others.

Prognosis

With rapid and adequate treatment and monitoring, the risk of morbidity and mortality is low. Rapid access to medical care and rapid acknowledge of the disease process are essential to patient prognosis. As stated above, the first hour after symptoms exposure is responsible for half of the related fatalities. [14],[17],[10]

Hospital admission is required in 4% or less of acute allergic reactions diagnosed in the emergency department. If epinephrine is required, as in cases of anaphylaxis, and complete resolution is noted. Emergency department (ED) observation for 4 hours is recommended. If no further intervention is required, the patient can be discharged home with a prescription for an epinephrine autoinjector and follow up is appropriate. If the patient requires airway intervention, is refractory to treatment, or is deemed unstable, admission to the intensive care unit (ICU) for close monitoring is advised. For patients with a history of biphasic reactions, severe reactions, beta-blocker use, elderly, those who live alone, or those with poor access to health care, or deemed at risk should be monitored longer.

Along with the prescription for an epinephrine pen, antihistamines and corticosteroids are appropriate for 3 to 5 days. If the inciting source is unknown and the patient will have a prolonged time before follow up, consider corticosteroid use for 1 to 2 weeks with an appropriate taper. Also consider writing for multiple epinephrine autoinjectors to ensure they are kept in various locations (home, school, work, vehicle). Educate and document the need for 24-hour access to the epinephrine autoinjector is symptoms begin to recur.

Patients with severe allergic reactions and anaphylaxis who take beta-blockers are at greater risk for prolonged or more severe symptoms; consider other classes of medication if possible. Patients may also consider obtaining medical alert bracelets or the like for assistance in the future.

Pearls and Other Issues

There is no absolute contraindication to treatment with epinephrine in anaphylaxis.

Treatment includes airway, decontamination, epinephrine 1:1000 0.3 to 0.5 mg IM, and a fluid bolus. Then start secondary treatments. Avoidance of the inciting agents is the key to prevention.

Patients should always be provided with an epinephrine auto-injector and instructed how to use it. Patients should also be given outpatient follow up with an allergist and immunologist to assist in the determination of inciting agent and prevention of future reoccurrences. Once the patient is stabilized, short-term desensitization procedures can be undertaken.

Enhancing Healthcare Team Outcomes

An evidence-based approach to anaphylaxis

Anaphylaxis is a rapid systemic and unpredictable disorder that is life-threatening. The disorder often occurs after exposure to certain antigens which in most cases are insect venom, food or medications. The condition is immune-mediated and rapidly induces symptoms. For those who have not encountered anaphylaxis, the diagnosis can be difficult. In the United States, the rates of anaphylaxis have doubled over the past 20 years, and at least 1500 people die from the disorder each year. The potentially life-threatening nature of the disorder makes it imperative that one be prepared and offer prompt treatment. This is one of the few medical disorders during which a health care worker does not have the luxury of time. Having epinephrine on hand can be life-saving if one wants to avoid a fatal outcome. However, despite considerable evidence that epinephrine is the drug of choice, it is under-used. Instead, many healthcare workers use an antihistamine, a drug which does not prevent or relieve all the manifestation of anaphylaxis.[18] In addition, the antihistamine does not even start to work for 1 to 3 hours depending on the route of administration. Given these findings, it is imperative that all healthcare workers be educated on anaphylaxis and its treatment. Evidence indicates that the following healthcare workers are critical for managing and preventing anaphylaxis.

Since people may develop anaphylaxis almost anywhere, it is important that all healthcare workers know the signs and symptoms of the disorder and know how to administer epinephrine.

The pharmacist is in a key position to educate the patient and family about anaphylaxis. Plus the pharmacist can teach the patient and family to carry epinephrine with them all the time

In addition, all physicians, nurses and other allied healthcare workers need to know the signs and symptoms of anaphylaxis and how to administer epinephrine.

The treating physician should try to reduce all the trigger factors and ensure optimal management of asthma.[19] (Level III)

Outcomes

Despite awareness of the seriousness of anaphylaxis, and treatment of anaphylaxis is not optimal. At least 1500 die each year from a condition that can be treated and even prevented. Although the seriousness of anaphylaxis is well established, there are no randomized trials to determine the effectiveness of antihistamines and how it compares to epinephrine. Further, what outcomes to measure after treatment have never been defined. In the absence of any solid clinical data, it is important that all healthcare workers are prepared to deal with anaphylaxis and know how to administer epinephrine.[20] (Level V)


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Anaphylaxis - Questions

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A patient is unresponsive with a swollen tongue completely obstructing the airway. Which immediate treatment is most appropriate?



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A patient is apneic as a consequence of anaphylactic shock. Which is the most appropriate initial treatment?



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A patient was stung by an insect at a picnic and given intramuscular epinephrine. On arrival in the emergency department, the patient is stridulous, dusky, and unable to speak. What should be the first treatment?



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A 28-year-old female arrives at the emergency department following a wasp sting. Her blood pressure is 80/58 mmHg, heart rate 130 beats/min, and respiratory rate 24 breaths/min. She is pale, diaphoretic, and wheezing bilaterally. What is the best initial treatment?



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A police officer with a known allergy to bee stings receives a sting while on traffic duty. In addition to intravenous fluids, what is the mainstay of treatment for anaphylaxis?



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What is the best advice for a patient with a history of acute anaphylactic reactions?



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A patient with anaphylaxis following a bee sting will not present with which of the following?



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Which finding is least likely during anaphylaxis?



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Which is least likely to be observed in an anaphylactic reaction?



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A 5-year-old boy has facial swelling, urticaria, and expiratory wheezing bilaterally. What is the most important drug to be administered immediately?



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What mediates anaphylaxis and airway constriction?



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Which is not normally seen in anaphylactic shock?



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Which of the following is not a reason that epinephrine is used for anaphylaxis?



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Which of the following is a mechanism of action of epinephrine in the emergency treatment of anaphylaxis?



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Which of the following drugs should be administered first to treat anaphylaxis following a bee sting?



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A 20-year-old female is stung by several bees and develops anaphylaxis. Paramedics administer 0.3 mg of epinephrine intramuscularly, but the patient required intubation and ventilation prior to reaching the emergency department. A second dose of epinephrine was administered but the patient remains hypotensive and tachycardic. Succinylcholine was administered prior to intubation. A ventilator is set at AC of 10, tidal volume of 450 ml, PEEP of 5 cmH2O, and FIO2 of 1.0. The cardiovascular exam shows tachycardia. Lungs show bilateral wheezes ending before the next inspiration. Normal saline is running at 1 liter per hour. Select the most appropriate treatment for her hypotension.



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What type of allergic reaction is implicated in anaphylactoid reaction following penicillin administration?



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A patient with dental pain was treated with penicillin and was observed to have acute swelling of his face and tongue and development of expiratory wheezing and generalized body rash. What is the most appropriate immediate management of this patient?



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What should be the first response to a patient presenting with hoarseness and wheals on the neck and arms following the ingestion of peanuts?



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A patient presents to the emergency department with the first episode of puffy eyelids, swollen lips, profound pruritus, and an audible wheeze. There was no history of insect sting nor food allergy. What is the most appropriate immediate treatment for this patient?



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Which condition is likely if a patient has an impending sense of doom followed by pruritus and flushing?



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A patient presents to the emergency department with hives, hypotension, and wheezing. What is the best initial step in management?



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Which of the following is not suggestive of anaphylaxis?



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What is the most common cause of anaphylaxis?



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Which of the following medications can be used to treat anaphylaxis?



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What medication may be used to prevent late-phase allergic reactions (biphasic anaphylaxis)?



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A patient presents with anaphylaxis. What is the next step in management after administering epinephrine?



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During anaphylaxis, what is the best treatment for bronchospasm refractory to epinephrine?



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What does urticaria with hypotension and bronchospasm indicate?



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Anaphylactic reactions involve which antibody class?



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An 8-year-old boy is stung by a bee and faints. He is pale, and his pulse is weak. What is the diagnosis?



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Which of the following is the most common trigger for anaphylaxis?



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Which of the following is not an appropriate preventative measure for penicillin-induced anaphylaxis?



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Which of the following is the most common drug causing anaphylaxis?



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Which of the following is a true statement about IgE-mediated anaphylaxis?



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What is the best initial management of anaphylaxis in an adult patient?



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Which is not a common cause of anaphylaxis?



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Which of the following should not immediately be given to a patient developing an anaphylactic reaction?



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A 12-year-old has just been given an allergy shot. He complains of chest discomfort and nausea. His voice is strained and muffled, and his face is flushed. What is the first priority in management?



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Which is not a common symptom in anaphylactic shock?



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What is the preferred route of administration of epinephrine when used for the treatment of anaphylaxis?



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How many allergy shot associated deaths in the United States are reported per year on average?



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What is the first treatment step for a patient complaining of respiratory distress after eating, who reports a significant peanut allergy?



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A patient suffers a rapid onset of severe cardiovascular and/or respiratory collapse after a minor incident such as drug or contrast administration or insect bite. What is the most likely diagnosis?



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A person develops an acute reaction as a result of something s/he ingested or injected. What is the term for this?



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A patient is treated in the emergency department for anaphylaxis. After recovery, which of the following instructions should be given to the patient at discharge?



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An 82-year-old male with multiple medical problems presents in anaphylactic shock. He was stung by a bee approximately 30 minutes prior to arrival. The patient was given 2 epinephrine auto-injectors without relief. On exam, he has hives, stridor, wheezing, and is vomiting. His BP is 92/55, RR 30, Sp02 91% and HR 55. What is the next best step in management?



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A patient is in anaphylactic shock and has stopped breathing. Which of the following is a recommended first approach to treatment?



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A 17-year-old male presents to the emergency department complaining of shortness of breath that started about 20 minutes ago after being stung by a bee on his arm. Vital signs reveal pulse 122 bpm, blood pressure 106/60 mmHg, respiratory rate 24/min and a pulse oximetry of 94% on room air. On exam, he has a diffuse urticarial rash, some swelling of the lips and tongue, and wheezing noted on auscultation. What is the most important initial treatment to administer?



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A 14-year-old boy with a history of allergy to yellow jackets is stung and immediately begins experiencing tightness in the chest and wheezing. What is the drug of choice for management of this child?



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A 40-year-old male presents after going to the dentist. He states that he had a tooth pulled and was placed on cephalexin. He received the anesthetic bupivacaine. He is complaining of shortness of breath and swelling of his lips and tongue. What should be the first step in the treatment of this patient?



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A nursing student is working in the emergency department as part of his final clinical rotation before graduating. As the student nurse follows his preceptor around, they enter the room of a client newly admitted from triage. The preceptor walks into the room and quickly assesses the client. The student notices a flurry of activity in the room by his preceptor. The client is red all over, dyspneic, has stridor, itching profusely, and has swelling around the eyes, lips, and portions of the tongue. The client's heart rate 132 beats/min, blood pressure 90/40 mmHg, respiratory rate 32, and pulse oximetry 88% on room air. All symptoms started after eating some peanuts 20 minutes before arrival. What are immediate actions needed based on this clinical scenario that the nurse can anticipate? Select all that apply.



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An 18-year-old was hiking stung by a bee, started wheezing, and lost consciousness. His friend called 911 and upon arrival of emergency medical services, his vitals were pulse 110 bpm, respiratory rate 10/minute, blood pressure 60/40 mmHg, and temperature 98.6 F. What should be next best step should be taken by the paramedic?



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A 20-year-old presented to the emergency department with shortness of breath, severe urticaria, facial flushing, after a bee sting. Which of the following is the mechanism of anaphylaxis secondary to a bee sting?



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Anaphylaxis - References

References

Okubo Y,Nochioka K,Testa MA, Nationwide Survey of Hospitalization Due to Pediatric Food-Induced Anaphylaxis in the United States. Pediatric emergency care. 2018 Aug 14     [PubMed]
Castilano A,Sternard B,Cummings ED,Shi R,Arnold T,Bahna SL, Pitfalls in anaphylaxis diagnosis and management at a university emergency department. Allergy and asthma proceedings. 2018 Jul 1     [PubMed]
Akenroye AT,Ajala A,Azimi-Nekoo E,de Vos GS, Prevalence of anaphylaxis among adults admitted to critical care for severe asthma exacerbation. Emergency medicine journal : EMJ. 2018 Aug 9     [PubMed]
Pattanaik D,Lieberman P,Lieberman J,Pongdee T,Keene AT,     [PubMed]
Mota I,Gaspar Â,Benito-Garcia F,Correia M,Chambel M,Morais-Almeida M, Drug-induced anaphylaxis: seven-year single-center survey. European annals of allergy and clinical immunology. 2018 Jul 20     [PubMed]
Yue D,Ciccolini A,Avilla E,Waserman S, Food allergy and anaphylaxis. Journal of asthma and allergy. 2018     [PubMed]
Parrish CP,Kim H, Food-Induced Anaphylaxis: an Update. Current allergy and asthma reports. 2018 Jun 14     [PubMed]
Protudjer JLP,Olén O,Vetander M,Kull I,Melén E,van Hage M,Wickman M,Bergström A, Milk-Related Symptoms and Immunoglobulin E Reactivity in Swedish Children from Early Life to Adolescence. Nutrients. 2018 May 21     [PubMed]
Anagnostou A, Anaphylaxis in children: epidemiology, risk factors and management. Current pediatric reviews. 2018 May 6     [PubMed]
Jimenez-Rodriguez TW,Garcia-Neuer M,Alenazy LA,Castells M, Anaphylaxis in the 21st century: phenotypes, endotypes, and biomarkers. Journal of asthma and allergy. 2018     [PubMed]
Valenta R,Karaulov A,Niederberger V,Gattinger P,van Hage M,Flicker S,Linhart B,Campana R,Focke-Tejkl M,Curin M,Eckl-Dorna J,Lupinek C,Resch-Marat Y,Vrtala S,Mittermann I,Garib V,Khaitov M,Valent P,Pickl WF, Molecular Aspects of Allergens and Allergy. Advances in immunology. 2018     [PubMed]
Graudins LV,Trubiano JA,Zubrinich CM,Elliott AS,Aung AK, Medication-related anaphylaxis treated in hospital: Agents implicated, patient outcomes, and management lessons. Pharmacoepidemiology and drug safety. 2018 Jul 27     [PubMed]
Aun MV,Kalil J,Giavina-Bianchi P, Adults and children with anaphylaxis in the emergency room: why it is not recognized? Current opinion in allergy and clinical immunology. 2018 Jul 16     [PubMed]
De Feo G,Parente R,Triggiani M, Pitfalls in anaphylaxis. Current opinion in allergy and clinical immunology. 2018 Jul 19     [PubMed]
Cohen N,Capua T,Pivko D,Ben-Shoshan M,Benor S,Rimon A, Trends in the diagnosis and management of anaphylaxis in a tertiary care pediatric emergency department. Annals of allergy, asthma     [PubMed]
Gallagher JL,Rivera RD,Van Shepard K,Roushan T,Ahsan G,Ahamed SI,Chiu A,Jurken M,Simpson PM,Nugent M,Gobin KS,Wen CKF,Eldredge CE, Life-Threatening Allergies: Using a Patient-Engaged Approach. Telemedicine journal and e-health : the official journal of the American Telemedicine Association. 2018 Jul 3     [PubMed]
Lindor RA,McMahon EM,Wood JP,Sadosty AT,Boie ET,Campbell RL, Anaphylaxis-related Malpractice Lawsuits. The western journal of emergency medicine. 2018 Jul     [PubMed]
Fineman SM, Optimal treatment of anaphylaxis: antihistamines versus epinephrine. Postgraduate medicine. 2014 Jul     [PubMed]
Leatherman BD, Anaphylaxis in the allergy practice. International forum of allergy     [PubMed]
Rubin T,Clayton J,Adams D,Jou H,Vohra S, Systematic review of outcome measures in trials of pediatric anaphylaxis treatment. BMC pediatrics. 2014 Jun 20     [PubMed]

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