Anaphylaxis Flashcards
How is anaphylaxis defined?
Anaphylaxis is an immediate severe allergic reaction following sequential exposure, leading to an immune (IgE) mediated mast cell and basophil degranulation. In general, it is defined by the severity of symptoms, not cause.
Here’s a list of common symptoms:
* Pruritic (Itchy) rash/hives
* Constriction of airways
* Swollen tongue
* Wheezing
* Dyspnea (Shortness of breath)
* Tachycardia/hypotension/shock
* Nausea/vomiting/diarrhea
* Syncope (fainting)
Anaphylaxis is diagnosed clinically based on presenting symptoms, highlighting the need to understand its pathophysiology and identify potential triggers or exposures. The fasted way to tell this apart from angioedema is with pruritus (itchiness), where anaphylaxis is pruritic and angioedema is not.
What is the first step in the process leading to anaphylaxis?
Initial sensitization to an antigen.
anaphylactoid rxn bypass this stage causing immediate systemic symptoms.
What is the progression from sensitization to death in anaphylaxis?
Sensitization → Re-exposure
Re-exposure → Mediator release
Mediator release → Symptoms
Symptoms → Death (if untreated)
What is the primary difference between anaphylaxis and anaphylactoid reactions?
Anaphylactoid reactions are not mediated by IgE but are clinically identical and treated the same way. Anaphylactoid reactions are severe pseudoallergic reactions with symptoms of anaphylaxis (e.g., rash, angioedema), due to vancomycin or opioid use) or complement-mediated mast cell degranulation.
What type of shock does anaphylaxis cause?
A form of distributive shock.
What type of hypersensitivity reaction is anaphylaxis?
Type 1
(immediate)
What happens upon re-exposure to the antigen in anaphylaxis?
IgE binds to mast cells, leading to the release of granules from mast cells and basophils in the cutaneous layers and blood vessels.
What immune mechanism mediates anaphylaxis?
IgE binds to mast cells, triggering the release of histamine, prostaglandins, and leukotrienes.
What mediators are released during anaphylaxis?
Histamine, leukotrienes, and prostaglandins.
What is the role of histamine in anaphylaxis?
Histamine increases vascular permeability and causes smooth muscle contraction, leading to symptoms like swelling and airway narrowing.
What is the role of leukotrienes in anaphylaxis?
They contribute to bronchoconstriction, increased vascular permeability, and inflammation.
How does prostaglandin contribute to anaphylaxis?
It amplifies inflammation and smooth muscle contraction, worsening airway constriction and hypotension.
What are the hallmark symptoms of anaphylaxis?
Organized in an “ABCDE” frame of mind (Airway, Breathing, Circulation, Disability, Exposure), think airway first:
Swollen tongue, airway constriction/obstruction, wheezing, dyspnea, or labored breathing.
Tachycardia, hypotension, dizziness, fainting, confusion, loss of consciousness.
Nausea, vomiting, and diarrhea.
Itchy rash, flushing, or hives.
Swelling.
Patients may require immediate intubation!
Are skin signs always present with anaphylaxis?
No, missing in ~10% of cases
How are the hemodynamics described in anaphylaxis?
Hypotensive state (<90 SBP) leading to weak thready pulses.
What happens to systemic vascular resistance (SVR) in anaphylaxis?
SVR decreases due to widespread vasodilation caused by histamine and other inflammatory mediators.
Patients require IV access and fluids along with continuous vital sign monitoring.
What happens to cardiac output (CO) in anaphylaxis?
Cardiac output initially increases as a compensatory response, but it may decrease in severe cases due to hypovolemia from fluid extravasation.
What happens to pulmonary capillary wedge pressure (PCWP) in anaphylaxis?
PCWP decreases because of fluid redistribution into the interstitial and extravascular spaces.
What happens to diffusion capacity of the lungs for carbon monoxide (DLCO) in anaphylaxis?
DLCO may decrease due to pulmonary edema caused by increased vascular permeability.
How does anaphylaxis affect preload?
Preload decreases due to venodilation and fluid leakage from the vascular compartment into tissues. Histamine causes vasodilation and increased vascular permeability, leading to reduced SVR and hypotension.
What effect does anaphylaxis have on venous return?
Venous return decreases due to systemic vasodilation and fluid extravasation into tissues.
What is the worst potential outcome of untreated anaphylaxis?
Death.
Respiratory support is a critical component in the management.
What are common triggers of anaphylaxis?
Insect stings, foods, medications, and latex.
Latex is a very important cause of anaphylaxis in healthcare workers.
What are some common foods known to produce an anaphylactic/anaphylactoid reaction?
Peanuts (nuts in general), milk, eggs, shellfish, white fish, food additives, chocolate, cotton seed oil, and berries.
What common medications are known to produce an anaphylactic/anaphylactoid reaction?
Penicillin, Tetracycline, cephalosporin, aminoglycosides, amphotericin B, nitrofurantoin and sulfa.
Aspirin, NSAIDs, insulin, tetanus and diphtheria toxoids.
Local anesthetics (procaine, lidocaine, novacaine).
Vitamins (thiamine, folic acid).
Phenytoin, lamotrigine.
Quinidine, rifampin.
What are some common antigens known to produce an anaphylactic/anaphylactoid reaction?
Latex, pollen, venom from insect bites ( wasps, hornets, yellow jackets, ants, gnats, flies, horse flies, mosquitoes, cockroaches, Miller moths, snake and spiders).
How is the diagnosis established for anaphalaxis?
- Clinical diagnosis, no specific test.
- Tryptase can be ordered but will not peak until 1 - 1.5 hours after symptoms.
What is the first step in management for a patient with anaphylaxis?
Ensure that the airway is patent.
Delivery of ventilations may be difficult because of bronchoconstriction, inflammation, increased mucus production, and increased resistance in the lower airway.
The management of the airway may require supplemental oxygen delivered at 15 mL per minute along with an airway adjunct. Start with a rebreather mask, then step up to positive pressure ventilations, and if necessary, endotracheal intubation (rapid sequence intubation).
What medications are used for rapid sequence intubation?
Rocuronium and succinylcholine are neuromuscular blocking agents typically used (along with a sedative) in RSI. Both cause complete paralysis, loss of upper airway tone, and cessation of all respiratory effort, which can lead to hypoxia and cardiac arrest if an airway is not secured immediately. Patients who have a difficult airway should instead undergo awake intubation, with preservation of spontaneous breathing (vs paralysis).
What is a reasonable option for establishing an airway in a patient with a difficult airway?
Patients with acute onset of respiratory distress, angioedema, and shock following likely allergen exposure leading to anaphylaxis and an unstable respiratory status (eg, tachypnea, hypoxia, stridor, wheezing) that are worsening despite appropriate treatment. This situation necessitates a definitive airway. In contrast to rapid sequence intubation (RSI), awake intubation (either nasotracheal or orotracheal) is the preferred method of intubation for patients with difficult airways with an upper airway obstruction (eg, swollen lips/tongue, stridor). In awake intubation, the patient independently maintains upper airway tone and spontaneous ventilation while the airway is visualized (typically using a fiberoptic endoscope) to determine whether intubation is possible. During RSI, a patient is fully anesthetized and paralyzed, causing loss of all upper airway tone, protective airway reflexes, and respiratory drive. If intubation is unsuccessful, as can occur in patients with difficult airways, the patient can rapidly become hypoxic and experience cardiac arrest. Ketamine, a phencyclidine derivative, is the preferred agent to use for awake intubations because it provides dissociation, amnesia, and analgesia (ie, dissociative anesthesia) while maintaining upper airway tone, protective airway reflexes, and respiratory drive. It also causes a sympathetic surge (by inhibiting reuptake of catecholamines) that increases blood pressure and causes bronchial smooth muscle relaxation, which are additional benefits in patients with hypotension and bronchospasm.
What is the standard of care first-line medication for anaphylaxis?
Intramuscular epinephrine.
IM EPI serves as an alpha and beta adrenergic receptor agonist to reverse the effects of histamine and restore systemic vascular resistance. Epinephrine increases SVR, improves cardiac output by increasing contractility and heart rate, and restores vascular tone. These vascular effects are due to alpha-1 (predominate action) and alpha-2 (inhibitory, limiting the amount of vascualr affect).
Beta-1 will increase cardiac contractility while Beta-2 will promote airway bronchodilation, reversing the bronchoconstriction.
EPI also is an anti-histamine.
Duration of action is ~10 min.
Adult = 0.3 mg / Children = 0.15 mg
After managing airway and giving EPI, what other interventions are used for the management of anaphylaxis?
Aggressive IV fluids
(2 large bore IVs)
Anti-histamines
(H1 blocker like diphenhydramine, H2 blocker like cimetidine).
Glucocorticoids
(methylprednisolone or hydrocortisone)
Position the patient appropriately and provide secondary support measures.
What is urticaria?
Urticaria is a sudden swelling of the superficial skin layers caused by allergic or physical triggers.
After initial interventions, what should be done to management anaphylaxis?
Evaluate the patient to see if adequate response. If the BP remains below 90 mmHg, SpO2 is less than 90%, or respiratory symptoms persist, repeat delivery of epinephrine. Up To 3 doses of epinephrine can be administered. If the response is still inadequate, patients may require IV epinephrine.
What is a potential dangerous condition that can occur following treatment of anaphylaxis?
A biphasic reaction.
How should patients be followed, what is the disposition following an anaphylactic reaction?
- If no biphasic reaction occurred, provide education on allergic reactions, prescribe IM epinephrine and refer to an allergen specialist.
-Monitor patients continuously if they have a biphasic reaction.
A 36-year-old woman presents to the emergency department for evaluation of shortness of breath. About 30 minutes ago the patient was stung by a bee while hiking and quickly became short of breath and vomited once. The patient has a known allergy to bee stings but misplaced her epinephrine auto-injector several months ago. Temperature is 37.0 °C (98.6°F), pulse is 112/min, blood pressure is 115/65 mmHg, respiratory rate is 22/min, and oxygen saturation is 90% on room air. The patient is not using accessory muscles but appears to have difficulty breathing. Lung auscultation reveals diffuse wheezes bilaterally. There is an urticarial rash on the bilateral upper extremities. Paramedics administered one dose of intramuscular epinephrine in the ambulance while en route to the hospital. Which of the following is the best next step in management?
This patient presenting with shortness of breath, vomiting, and an urticarial rash after exposure to a known inciting agent has anaphylaxis. Anaphylaxis refers to an acute, potentially life-threatening allergic reaction that occurs upon second exposure after sensitization to an antigen. IgE-mediated activation of basophils and mast cells leads to the release of pro-inflammatory mediators (e.g., histamine, prostaglandins, cytokines). These mediators cause an overwhelming systemic inflammatory reaction that can ultimately result in anaphylactic shock or even death. If anaphylaxis is suspected, intramuscular epinephrine should be administered immediately (typically in the lateral thigh), even before obtaining a history and physical examination. Epinephrine raises blood pressure, reduces bronchospasm, and counteracts other effects of circulating inflammatory mediators. It is important for clinicians to recognize that patients may need multiple doses of epinephrine (up to 3). Administration of IV fluids may be necessary to maintain blood pressure in patients with anaphylaxis; however, this patient is not currently hypotensive. This patient should immediately be given a second dose of epinephrine since symptoms have not resolved with the first dose. Most patients respond to a single dose of IM epinephrine, particularly if it is given promptly after the onset of symptoms. IM epinephrine may be repeated at 5- to 15-minute intervals if there is no response or inadequate response. In severe cases where IM epinephrine is inadequate, a slow, continuous infusion of epinephrine can be used. H1 and H2 antihistamines and corticosteroids can be given as adjunctive therapy with epinephrine but they should not be given alone. They do not prevent or treat bronchoconstriction or hypotension that can be associated with anaphylaxis.
What are the primary triggers for urticaria?
Insect bites, medications, pressure (dermatographism), cold, vibration, and foods.
What are the first-line treatments for urticaria?
Antihistamines (e.g., diphenhydramine, loratadine, hydroxyzine, fexfenadine, cetirizine+cimetidine)
Leukotriene receptor antagonists (montelukast or zafirlukast).
How is urticaria related to anaphylaxis?
Urticaria can be a component of anaphylaxis, presenting as widespread wheals or a rash.
What is pressure urticaria, and how does it occur?
Pressure urticaria is triggered by physical pressure, causing mast cell degranulation.
What symptoms characterize allergic rhinitis?
Sneezing, itchy nose, watery eyes, pale or violaceous nasal turbinates, and nasal polyps.
How is allergic rhinitis typically diagnosed?
Clinically, based on recurrent episodes of characteristic symptoms, though skin or blood testing may confirm allergen-specific IgE levels.
What is the treatment of choice for allergic rhinitis?
Intranasal corticosteroids and antihistamines.
What environmental modifications help control allergic rhinitis?
Use of air purifiers, allergen-proof mattress covers, and avoiding exposure to known allergens.
What is a significant finding on nasal smear in allergic rhinitis?
Increased eosinophils.
