Anaphylaxis

Question 1

How is anaphylaxis defined?

Answer 1

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.

Question 2

What is the first step in the process leading to anaphylaxis?

Answer 2

Initial sensitization to an antigen.

anaphylactoid rxn bypass this stage causing immediate systemic symptoms.

Question 3

What is the progression from sensitization to death in anaphylaxis?

Answer 3

Sensitization → Re-exposure

Re-exposure → Mediator release

Mediator release → Symptoms

Symptoms → Death (if untreated)

Question 4

What is the primary difference between anaphylaxis and anaphylactoid reactions?

Answer 4

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.

Question 5

What type of shock does anaphylaxis cause?

Answer 5

A form of distributive shock.

Question 6

What type of hypersensitivity reaction is anaphylaxis?

Answer 6

Type 1
(immediate)

Question 7

What happens upon re-exposure to the antigen in anaphylaxis?

Answer 7

IgE binds to mast cells, leading to the release of granules from mast cells and basophils in the cutaneous layers and blood vessels.

Question 8

What immune mechanism mediates anaphylaxis?

Answer 8

IgE binds to mast cells, triggering the release of histamine, prostaglandins, and leukotrienes.

Question 9

What mediators are released during anaphylaxis?

Answer 9

Histamine, leukotrienes, and prostaglandins.

Question 10

What is the role of histamine in anaphylaxis?

Answer 10

Histamine increases vascular permeability and causes smooth muscle contraction, leading to symptoms like swelling and airway narrowing.

Question 11

What is the role of leukotrienes in anaphylaxis?

Answer 11

They contribute to bronchoconstriction, increased vascular permeability, and inflammation.

Question 12

How does prostaglandin contribute to anaphylaxis?

Answer 12

It amplifies inflammation and smooth muscle contraction, worsening airway constriction and hypotension.

Question 13

What are the hallmark symptoms of anaphylaxis?

Answer 13

Organized in an “ABCDE” frame of mind (Airway, Breathing, Circulation, Disability):

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.

Question 14

Are skin signs always present with anaphylaxis?

Answer 14

No, missing in ~10% of cases

Question 15

How are the hemodynamics described in anaphylaxis?

Answer 15

Hypotensive state (<90 SBP) leading to weak thready pulses.

Question 16

What happens to systemic vascular resistance (SVR) in anaphylaxis?

Answer 16

SVR decreases due to widespread vasodilation caused by histamine and other inflammatory mediators.

Question 17

What happens to cardiac output (CO) in anaphylaxis?

Answer 17

Cardiac output initially increases as a compensatory response, but it may decrease in severe cases due to hypovolemia from fluid extravasation.

Question 18

What happens to pulmonary capillary wedge pressure (PCWP) in anaphylaxis?

Answer 18

PCWP decreases because of fluid redistribution into the interstitial and extravascular spaces.

Question 19

What happens to diffusion capacity of the lungs for carbon monoxide (DLCO) in anaphylaxis?

Answer 19

DLCO may decrease due to pulmonary edema caused by increased vascular permeability.

Question 20

How does anaphylaxis affect preload?

Answer 20

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.

Question 21

What effect does anaphylaxis have on venous return?

Answer 21

Venous return decreases due to systemic vasodilation and fluid extravasation into tissues.

Question 22

What is the worst potential outcome of untreated anaphylaxis?

Answer 22

Death.

Respiratory support is a critical component in the management.

Question 23

What are common triggers of anaphylaxis?

Answer 23

Insect stings, foods, medications, and latex.

Latex is a very important cause of anaphylaxis in healthcare workers.

Question 24

What are some common foods known to produce an anaphylactic/anaphylactoid reaction?

Answer 24

Peanuts (nuts in general), milk, eggs, shellfish, white fish, food additives, chocolate, cotton seed oil, and berries.

Question 25

What common medications are known to produce an anaphylactic/anaphylactoid reaction?

Answer 25

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.

Question 26

What are some common antigens known to produce an anaphylactic/anaphylactoid reaction?

Answer 26

Latex, pollen, venom from insect bites ( wasps, hornets, yellow jackets, ants, gnats, flies, horse flies, mosquitoes, cockroaches, Miller moths, snake and spiders).

Question 27

How is the diagnosis established for anaphalaxis?

Answer 27

Clinical diagnosis, no specific test.

Question 28

What is the first step in management for a patient with anaphylaxis?

Answer 28

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).

Question 29

What is the standard of care first-line medication for anaphylaxis?

Answer 29

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

Question 30

After managing airway and giving EPI, what other interventions are used for the management of anaphylaxis?

Answer 30

Aggressive IV fluids
(2 large bore IVs)

Anti-histamines
(H1 blocker like diphenhydramine, H2 blocker like cimetidine).

Glucocorticoids
(methylprednisolone or hydrocortisone)

Question 31

What is urticaria?

Answer 31

Urticaria is a sudden swelling of the superficial skin layers caused by allergic or physical triggers.

Question 32

What are the primary triggers for urticaria?

Answer 32

Insect bites, medications, pressure (dermatographism), cold, vibration, and foods.

Question 33

What are the first-line treatments for urticaria?

Answer 33

Antihistamines (e.g., diphenhydramine, loratadine, hydroxyzine, fexfenadine, cetirizine+cimetidine)

Leukotriene receptor antagonists (montelukast or zafirlukast).

Question 34

How is urticaria related to anaphylaxis?

Answer 34

Urticaria can be a component of anaphylaxis, presenting as widespread wheals or a rash.

Question 35

What is pressure urticaria, and how does it occur?

Answer 35

Pressure urticaria is triggered by physical pressure, causing mast cell degranulation.

Question 36

What symptoms characterize allergic rhinitis?

Answer 36

Sneezing, itchy nose, watery eyes, pale or violaceous nasal turbinates, and nasal polyps.

Question 37

How is allergic rhinitis typically diagnosed?

Answer 37

Clinically, based on recurrent episodes of characteristic symptoms, though skin or blood testing may confirm allergen-specific IgE levels.

Question 38

What is the treatment of choice for allergic rhinitis?

Answer 38

Intranasal corticosteroids and antihistamines.

Question 39

What environmental modifications help control allergic rhinitis?

Answer 39

Use of air purifiers, allergen-proof mattress covers, and avoiding exposure to known allergens.

Question 40

What is a significant finding on nasal smear in allergic rhinitis?

Answer 40

Increased eosinophils.