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Immune / Infectious

Anaphylaxis & Hypersensitivity Reactions

High-yield Verified · Sep 2026

Anaphylaxis is a rapidly evolving, generalized, multi-system allergic reaction — an acute hypersensitivity emergency that can begin within minutes of exposure and quickly become life-threatening.

One page, two payloads: the four Gell–Coombs hypersensitivity types every exam maps, and the type I emergency itself — recognition even without hives, IM epinephrine before anything else, positioning that prevents sudden death, and the biphasic return no one expects.

What’s going wrong in the body

The normal physiology, where it fails, and why the body’s compensation backfires.

01 Four ways the immune system overreacts

Hypersensitivity is a normal immune apparatus aimed at the wrong target, and the Gell–Coombs classification sorts the damage by mechanism. Type I (immediate) is IgE bound to mast cells reacting within minutes to typically harmless environmental antigens — anaphylaxis, allergic asthma, allergic rhinitis, food allergy, urticaria and angioedema. Type II (cytotoxic) is IgG or IgM antibody binding antigens on cell surfaces, destroying the cell through complement (the membrane attack complex), C3b-tagged phagocytosis, or NK-cell killing — the hemolytic transfusion reaction, autoimmune hemolytic anemia, hemolytic disease of the newborn, Goodpasture disease, immune thrombocytopenia.

Type III (immune complex) is circulating antigen–antibody complexes depositing in skin, joints and kidneys, where complement (C3a/C5a) summons neutrophils that injure the tissue — serum sickness (beginning 1–2 weeks after first exposure), lupus nephritis, and post-streptococcal glomerulonephritis. Type IV (delayed) has no antibody at all: sensitized T cells and their cytokines drive inflammation that typically appears 48–72 hours after exposure — contact dermatitis (poison ivy, nickel), the tuberculin (PPD) skin test, granulomatous inflammation, and severe drug reactions like SJS/TEN. The timing is the exam tell: minutes = I, days = IV.

The Gell–Coombs map: one antigen, four mechanisms — sorted by what attacks (IgE, IgG/IgM, immune complexes, T cells) and how fast.

02 The silent setup: sensitization

Anaphylaxis is the classic type I reaction, and it takes two exposures to build. The first exposure causes no symptoms: antigen-presenting cells activate T-helper cells, T-helper cells push B cells to produce allergen-specific IgE, and that IgE docks onto high-affinity FcεRI receptors on mast cells and basophils. The patient walks away sensitized — armed — and has no idea.

On re-exposure, the allergen cross-links the IgE already sitting on mast cells and basophils, and the cells degranulate: histamine, tryptase, carboxypeptidase A and proteoglycans dump out preformed, while leukotrienes, prostaglandins and platelet-activating factor are newly synthesized. This is why the "first dose was fine" history is worthless reassurance — the fine first dose is exactly what loaded the weapon.

Two-phase mechanism: a symptomless first exposure arms the mast cells with IgE; re-exposure cross-links it and triggers degranulation.

03 The mediator storm: three fronts at once

The released mediators attack on parallel fronts, and each maps to a bedside finding. Histamine drives vasodilation and increased vascular permeability → tissue hypoperfusion; prostaglandin D constricts bronchi; leukotrienes and PAF do both — bronchoconstriction plus more capillary leak. The net result is the anaphylaxis triad: vasodilation + capillary leak (hypotension, urticaria, angioedema), bronchospasm (wheeze), and upper-airway swelling — with GI cramping, vomiting and diarrhea riding along. Onset is fast: usually within 1 hour of exposure, often within seconds to minutes.

The circulatory collapse is distributive shock: the vessels dilate and leak until the central vascular compartment is effectively empty. That single mechanism explains two core interventions — lay the patient supine with the legs elevated to keep what volume remains in the central circulation, and give epinephrine, whose alpha-1 vasoconstriction directly reverses the dilation and leak while its beta effects open the bronchi.

The three-front assault: one degranulation event simultaneously empties the vessels, closes the airways, and cramps the gut.

04 Why it isn’t over when it’s over

Type I reactions carry a late phase: hours after the initial mediator burst, recruited eosinophils and T cells can make symptoms persist or recur. Clinically this shows up as the biphasic reaction — symptoms return after apparent resolution, without any re-exposure — in up to 20% of cases (clinically significant in 4–5%), peaking 8–11 hours after the initial reaction. This is the entire rationale for the observation window and for warning every discharged patient that "better" is not the same as "done."

The stakes justify the urgency: anaphylaxis has a lifetime prevalence of about 1–3%, causes at least 1,500 US deaths per year, and kills fewer than 0.5% of patients who reach an emergency department or hospital — and half of all fatalities occur within the first hour. With rapid, adequate treatment and monitoring, though, the risk of morbidity and mortality is low. The window is short; the outcome inside it is excellent.

Causes & risk factors

Modifiable factors are teaching targets — the patient can act on them.

Foods — peanuts especially; tree nuts, fish, shellfish, milk, eggs, wheat, soy, sesame, red meat (regional patterns: peanut/tree nut in North America–Australia, shellfish in Asia, sesame in the Middle East) modifiable Insect stings (bee, fire ant venom) Medications — with foods and venom, one of the three most frequent trigger groups worldwide (WAO) modifiable Natural rubber latex modifiable Radiocontrast media & medical dyes modifiable Perioperative agents Allergen immunotherapy injections Exercise (an additional cause in its own right) Amplifying cofactors — physical exercise, infection, psychological stress, sleep deprivation, alcohol modifiable Pollen and inhaled allergens rarely cause anaphylaxis

Signs & symptoms

Each finding tied to the mechanism that produces it — and the triage it calls for.

Generalized urticaria (hives), itching, flushing early Report immediately
Why: Histamine-driven vasodilation and capillary leak in the skin — present in ~90% of patients, usually among the earliest cues.
Angioedema — swollen lips, tongue, uvula; periorbital edema Report immediately
Why: The same capillary leak pouring into deeper tissue. Perioral and tongue swelling sit next to the airway — treat as an airway threat, not a skin finding.
Throat tightness, voice change, stridor Report immediately
Why: Laryngeal edema narrowing the upper airway. Once swelling starts, every minute of delay makes intubation harder — "obtaining a definitive airway is imperative."
Wheeze, cough, dyspnea (respiratory involvement in ~85%) Report immediately
Why: Leukotriene-, prostaglandin-D- and PAF-mediated bronchoconstriction on top of upper-airway angioedema.
Hypoxemia (falling SpO₂) Report immediately
Why: Bronchospasm below plus a narrowing airway above — the reason high-flow oxygen goes on early.
Hypotension — SBP < 90 mm Hg or > 30% below the patient’s baseline Report immediately
Why: Vasodilation plus capillary leak empties the central circulation: distributive shock. This threshold is itself a diagnostic criterion (WAO 2020).
Tachycardia with a weak pulse Report immediately
Why: The heart races to compensate for a vascular compartment that has dilated and leaked its volume away.
Dizziness, syncope, incontinence Report immediately
Why: End-organ hypoperfusion — the brain and sphincters losing pressure. These count as end-organ dysfunction in the diagnostic criteria.
Nausea, vomiting, painful cramps, diarrhea (GI symptoms in 25–30%) Report immediately
Why: Mediator effects on the gut. Persistent GI symptoms are one of the organ systems that satisfy the diagnostic criteria — not an innocent bystander.
No skin findings at all (~10% of cases)
Why: Urticaria may resolve before the patient presents, and WAO criterion 2 applies "even in the absence of typical skin involvement." Waiting for hives before treating is how anaphylaxis gets missed.
Shock and loss of consciousness late Report immediately
Why: The end of the distributive spiral: the empty circulation can no longer perfuse the brain.
Symptoms returning hours after resolution — without re-exposure late Report immediately
Why: The biphasic reaction (up to 20% of cases, peaking 8–11 hours after the first): recruited late-phase cells re-ignite the response.

Diagnostics

Test In this disorder Normal
Clinical criteria (the diagnosis itself) Anaphylaxis is a clinical diagnosis — no laboratory test is required. Treat on recognition; never wait on labs Anaphylaxis is highly likely with EITHER (1) acute onset (minutes–hours) of skin/mucosal involvement PLUS ≥ 1 of respiratory compromise, reduced BP or end-organ dysfunction, or severe GI symptoms — OR (2) acute hypotension, bronchospasm, or laryngeal involvement after a known/probable allergen, even without skin findings WAO 2020 —
Blood pressure Know the admission baseline — a "normal-looking" 92/60 is criterion-level hypotension in a patient who runs 140/85 SBP < 90 mm Hg or a > 30% drop from that patient’s baseline defines the hypotension criterion (children < 10 y: SBP < 70 + [2 × age in years]) WAO 2020 SBP ≥ 90 and within 30% of baseline
Serum tryptase Timing is the nursing job: draw within 15 minutes–3 hours of symptom onset; it may remain elevated up to 6 hours Elevated — supportive evidence of mast-cell degranulation, not required for diagnosis StatPearls —
Pulse oximetry (SpO₂) High-flow oxygen (preferably 100% via non-rebreather) for any respiratory distress and for anyone needing repeated epinephrine doses (WAO 2020) Hypoxemia with respiratory involvement — one of the findings that satisfies the respiratory-compromise criterion —

Complications

Warning: Laryngeal edema → airway obstruction Report immediately
Perioral edema, stridor, and angioedema are very high risk — the airway can swell shut.
"Obtaining a definitive airway is imperative": every minute of delay lets swelling progress, reducing the chance of successful intubation and raising the risk of a surgical airway. Voice change, throat tightness or stridor is a call-anesthesia-now cue, not a watch-and-wait one.
Warning: Distributive shock & death in the first hour Report immediately
Vasodilation and capillary leak collapse the circulation; half of anaphylaxis fatalities occur within the first hour.
This number is the entire argument for epi first, fast: IM epinephrine on recognition, supine with legs elevated, wide-bore IV access, and a 1–2 L (or 10–20 mL/kg) isotonic crystalloid bolus for hypotension. Delay — including delay spent giving antihistamines — is the modifiable risk.
Warning: Refractory anaphylaxis Report immediately
No response to repeated IM epinephrine doses — the reaction is outrunning intermittent dosing.
Escalates to IV epinephrine (initial 0.1 mg of 1:10,000 over 5–10 minutes, then an infusion from 1 µg/min titrated to effect) and ICU-level care. A patient on beta-blockers who responds poorly may receive glucagon, which bypasses the blocked beta receptor. Anticipate the escalation — don’t keep repeating what isn’t working.
Caution: Biphasic reaction Report immediately
Symptoms return after apparent resolution, without re-exposure — in up to 20% of cases (clinically significant in 4–5%), peaking 8–11 hours later.
The reason discharge is not the end of care: observe in the ED for at least 4 hours — longer after severe reactions or those needing multiple epinephrine doses (WAO 2020) — and send every patient home warned that returning symptoms mean emergency care immediately.

Medications for this condition

Why each class is prescribed here — every card links to its full pharmacology page.

Vasopressors & Inotropes First-line High-alert
Cardiovascular · norepinephrine

Epinephrine is THE drug of anaphylaxis — given first, immediately on recognition: its alpha-1 vasoconstriction reverses the vasodilation and capillary leak while its beta effects reverse the bronchospasm. Adult dose 0.3–0.5 mg IM (1 mg/mL) in the mid-anterolateral thigh (pediatric 0.01 mg/kg, max 0.5 mg), repeatable every 5–15 minutes (WAO 2020) — about 35% of patients need a second dose. There is no absolute contraindication in anaphylaxis. Refractory cases escalate to a low-dose IV epinephrine infusion in the ICU.
Antihistamines
Respiratory · diphenhydramine (1st-gen)

Adjunct only — never first, never a reason epinephrine waits. H1 (diphenhydramine 25–50 mg IV/IM) plus H2 (famotidine 20 mg IV) relieve the cutaneous and minor allergic symptoms, but their benefit in anaphylaxis itself is unproven, and WAO warns they can delay the intervention that saves lives: repeated IM epinephrine. Giving diphenhydramine first is the classic exam trap.
Corticosteroids
Endocrine · prednisone

Adjunct only, and increasingly debated. Methylprednisolone 80–125 mg IV (or hydrocortisone 250–500 mg IV) acutely, then oral prednisone 40–60 mg/day for 3–5 days; StatPearls frames the rationale as reducing the length or biphasic response of anaphylaxis, but WAO 2020 cites increasing evidence of no benefit in acute management — possibly harm — making routine use controversial. Whatever the verdict, a steroid never delays epinephrine.

Beyond medications

  • Stop the trigger — halt the running infusion or transfusion, remove the exposure. It takes seconds and stops the antigen supply feeding the reaction.
  • Position: supine with lower extremities elevated — preserves the leaked-out circulation’s remaining volume centrally. Patients must not sit up, stand, or walk until clearly stabilized, even if they feel better: sitting up too soon risks empty ventricle syndrome, a profound fall in blood pressure that can be fatal (Canadian anaphylaxis review, 2024; NHS). Respiratory distress → sitting may optimize breathing (WAO 2020), raising the shoulders or sitting up slowly; pregnant → semi-recumbent on the left side; unconscious → recovery position (WAO 2020).
  • High-flow oxygen — preferably 100% via non-rebreather — for all respiratory distress and anyone receiving repeated epinephrine doses (WAO 2020).
  • Wide-bore IV access (14–16 gauge) + crystalloid bolus — 1–2 L or 10–20 mL/kg isotonic crystalloid for hypotension (WAO: 20 mL/kg for cardiovascular instability): distributive shock needs volume as well as vasoconstriction.
  • Inhaled beta-agonists for wheeze — albuterol (alone or with ipratropium) for bronchospasm; IV magnesium for refractory wheeze. Bronchodilators treat the lower airway only — they do nothing for laryngeal edema or shock.
  • Observe at least 4 hours after resolution — longer after severe reactions or multiple epinephrine doses (WAO 2020) — because the biphasic recurrence peaks 8–11 hours out.

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Assessment & monitoring
Assess in ABC order: airway first — listen for voice change, throat tightness, stridor; inspect lips, tongue and uvula for swelling.
Why: Laryngeal edema is the finding that kills fastest and closes the intubation window as it progresses — "obtaining a definitive airway is imperative," so these cues escalate immediately.
Then breathing: wheeze, cough, respiratory rate, continuous SpO₂.
Why: Respiratory involvement occurs in ~85%; bronchospasm plus upper-airway narrowing drives the hypoxemia that oxygen and epinephrine must reverse.
Then circulation: BP against the criterion (SBP < 90 or > 30% below baseline), pulse quality, mentation. Begin CPR if there is no pulse or breathing.
Why: Distributive shock declares itself as criterion-level hypotension, a weak rapid pulse, and a brain losing perfusion (dizziness, syncope, confusion).
Do not rule out anaphylaxis because the skin is clear.
Why: ~10% of cases have no skin findings, urticaria may fade before presentation, and WAO criterion 2 needs no skin involvement at all — hypotension or bronchospasm after a probable allergen is enough.
If tryptase is ordered, draw it within 15 minutes–3 hours of symptom onset.
Why: The level supports the diagnosis afterward but falls quickly (elevated up to ~6 hours) — and it is never a reason to delay treatment.
Escalate immediately for: stridor or perioral/tongue swelling · criterion-level hypotension · symptoms returning after resolution · no response to repeated epinephrine.
Why: These four cues map to the four killers: airway loss, distributive shock, the biphasic reaction, and refractory anaphylaxis needing IV epinephrine.
The first minutes (the reaction in front of you)
Give IM epinephrine first — before anything else: 0.3–0.5 mg (1 mg/mL) into the mid-anterolateral thigh (vastus lateralis), on recognition.
Why: Half of fatalities occur within the first hour, epinephrine is the only drug that reverses the mechanism, and there is no absolute contraindication. Antihistamines and steroids have unproven benefit and giving them first delays the drug that works.
Stop any running infusion or other ongoing exposure the moment the reaction is recognized.
Why: Medications are among the most frequent triggers worldwide; every additional milliliter is more antigen cross-linking more IgE.
Lay the patient supine with legs elevated — and never let them abruptly sit or stand, even to help.
Why: The dilated, leaking circulation needs every bit of venous return; sitting up before the patient is clearly stabilized risks empty ventricle syndrome — a profound fall in blood pressure that can be fatal (Canadian anaphylaxis review, 2024).
Apply high-flow oxygen, establish wide-bore (14–16 g) IV access, and run the ordered crystalloid bolus (1–2 L or 10–20 mL/kg) for hypotension.
Why: The shock is distributive: the fix is vasoconstriction (epinephrine) plus volume (fluids) plus oxygen across the narrowed airways.
Repeat epinephrine every 5–15 minutes (WAO 2020) if symptoms persist; anticipate escalation to an IV epinephrine infusion if there is no response.
Why: About 35% of patients need a second dose; a reaction refractory to repeated IM dosing is an ICU-level emergency, not a reason to repeat the same step a fourth time.
Add antihistamines and corticosteroids only after epinephrine, as ordered.
Why: The adjuncts treat comfort and skin, not the airway or the shock — WAO 2020 gives H1-antihistamines only "a limited role" and warns they can delay repeat epinephrine.
Patient teaching (before the next reaction)
Teach auto-injector technique: press the tip perpendicular against the mid outer thigh and hold (about 3–10 seconds; at least 5 per device teaching) — through clothing in an emergency if needed.
Why: The mid-anterolateral thigh is the guideline site; hesitation and wrong-site injection are the common failures. Expect tremulousness and palpitations afterward — that is the epinephrine working, not an allergic reaction to it.
Call 911 / get emergency care immediately after every injection, and stay lying down while waiting: no standing or walking, even if feeling better.
Why: The injection buys time; it does not replace emergency care — and resting avoids the sudden postural shift that can collapse an empty circulation.
Carry two auto-injectors, and consider keeping devices in multiple locations.
Why: About 35% of patients need a second epinephrine dose when symptoms continue or return; one device is half a plan.
Store devices in their carrier tube at room temperature, not refrigerated and away from light and extreme heat or cold; replace them before the expiration date; review the device instructions with the patient and caregivers.
Why: A degraded or expired device fails at the only moment it matters — and during a reaction the patient may need someone else to inject, so caregivers must know how.
Warn explicitly: symptoms can return hours after treatment — if they do, seek emergency care immediately.
Why: Biphasic reactions strike up to 20% of patients, peaking 8–11 hours after the first reaction, with no re-exposure needed.
Strictly avoid identified triggers, follow up with an allergist/immunologist to identify the inciting agent, and wear a medical alert ID naming the allergy.
Why: Trigger exposure is the one modifiable element; allergen immunotherapy may be considered for long-term desensitization in select patients — and the ID speaks when the patient can’t.
For insect stings: brush or scrape the stinger out sideways with a fingernail or the edge of a card — never tweezers.
Why: Pulling a stinger out with tweezers can squeeze more venom into the skin; S1 lists removing any stinger among the first steps.

How a real nurse thinks

The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.

  1. 1
    Recognize cues

    The cues that matter: a first dose of a new IV medication 5 minutes ago (a likely antigen), hives + lip swelling (skin/mucosa), hoarse voice + throat tightness + wheeze (respiratory, with the voice change pointing at the larynx), BP 82/48 against a baseline of 124/76 (both < 90 and > 30% below baseline), SpO₂ 91%, and GI cramping with nausea. The normal temperature and her anxiety are background.

  2. 2
    Analyze cues

    This satisfies the WAO criteria twice over: acute skin/mucosal involvement plus respiratory compromise plus hypotension — after a probable allergen. Mechanistically the mast cells have degranulated: vasodilation and capillary leak are emptying her circulation (distributive shock), while leukotrienes and prostaglandin D close her lower airways and laryngeal edema threatens the upper one. The hoarse voice is the most dangerous single cue: the airway is swelling now.

  3. 3
    Prioritize

    Epinephrine outranks everything else in the drawer. Half of anaphylaxis deaths occur within the first hour, and epinephrine is the only agent that reverses the mechanism. The diphenhydramine on the PRN list is the trap — its benefit in anaphylaxis is unproven and reaching for it first delays the drug that works. Sequence: stop the antigen → epinephrine IM → position → oxygen → escalate.

  4. 4
    Generate solutions

    Stop the antibiotic infusion (seconds, removes the ongoing antigen). Give epinephrine 0.3–0.5 mg IM in the mid-anterolateral thigh per protocol. Lay her supine with legs elevated — no sitting up, however much she wants to. High-flow oxygen for the SpO₂ of 91%. Activate the rapid response and notify the provider: anticipate wide-bore IV access with a 1–2 L crystalloid bolus for the hypotension, repeat epinephrine every 5–15 minutes if symptoms persist, airway support for the hoarse voice, and adjunct antihistamine/steroid after epinephrine. Nothing by mouth while her breathing is compromised.

  5. 5
    Take action

    Stop the infusion, inject epinephrine IM in the thigh, position supine with legs raised, apply oxygen, and call the rapid response with SBAR: "First dose of a new IV antibiotic started 5 minutes ago — hives, lip swelling, hoarse voice, wheeze, BP 82/48 from a baseline of 124/76, SpO₂ 91%. Infusion stopped, epinephrine 0.3 mg IM given at 1036, patient supine with legs elevated on oxygen. Requesting immediate evaluation; anticipate fluids and possible repeat epinephrine." Keep her flat — explain why she cannot suddenly sit up even when she feels better.

  6. 6
    Evaluate

    Success looks like: BP climbing back toward baseline, the wheeze and hoarseness resolving, SpO₂ recovering on oxygen, hives fading. Symptoms persisting at 5–15 minutes → repeat epinephrine (about a third of patients need a second dose); no response to repeated doses → refractory anaphylaxis, anticipate an ICU-level IV epinephrine infusion. Even a full recovery buys observation, not discharge: at least 4 hours of monitoring, with the biphasic warning delivered before she leaves.

Scenario — you’re the nurse

Work each question before revealing the answer. Rationales explain the wrong options too.

Med-surg unit · 1035, five minutes into a scheduled IV antibiotic

A 34-year-old woman admitted for cellulitis, receiving the first dose of a newly ordered IV antibiotic, started at 1030. Admission vitals this morning: BP 124/76, HR 78. She presses the call light: "My throat feels tight and I feel really strange."

1035 vitals — HR 118 · BP 82/48 (admission baseline 124/76) · RR 28 · SpO₂ 91% on room air · T 37.1 °C
Assessment — flushed; raised hives spreading across chest and arms; lips beginning to swell; voice hoarse; audible expiratory wheeze; nauseated with abdominal cramping; anxious but oriented
Infusion — antibiotic running at the ordered rate, ~5 minutes infused
Available PRNs — diphenhydramine IV; epinephrine 1 mg/mL in the emergency supply per anaphylaxis protocol
Q1 Select all that apply
Five minutes into the first dose of a new IV antibiotic, which findings support a diagnosis of anaphylaxis? Select all that apply.
  1. A. Raised hives spreading across the chest and arms with lip swelling
  2. B. Hoarse voice, throat tightness, and audible wheeze
  3. C. BP 82/48 mm Hg (admission baseline 124/76)
  4. D. Temperature 37.1 °C
  5. E. Nausea with painful abdominal cramping
Reveal answer & rationale
Answer: A, B, C, E
Anaphylaxis is a multi-system diagnosis: skin/mucosal involvement (A), respiratory compromise with laryngeal warning signs (B), criterion-level hypotension — SBP < 90 and more than 30% below her baseline (C), and GI symptoms, which count as an involved system (E). Acute onset after a probable allergen with these systems involved satisfies the WAO criteria. A temperature of 37.1 °C (D) is normal and contributes nothing — anaphylaxis is not a febrile reaction.
Q2 Multiple choice
Diphenhydramine IV is on the PRN list and closer at hand than the emergency supply. Which medication does the nurse give first?
  1. A. Diphenhydramine IV — it directly blocks the histamine driving the reaction
  2. B. Epinephrine 0.3–0.5 mg IM in the mid-anterolateral thigh
  3. C. Methylprednisolone IV to prevent a biphasic reaction
  4. D. An albuterol nebulizer for the audible wheeze
Reveal answer & rationale
Answer: B
Epinephrine first, always (B): it is the only drug that reverses the mechanism — alpha-1 vasoconstriction against the vasodilation and leak, beta effects against the bronchospasm — and half of fatalities occur within the first hour. Antihistamines (A) have unproven benefit in anaphylaxis and reaching for them first delays epinephrine — the classic trap. Steroids (C) are a debated adjunct that never comes first. Albuterol (D) treats only lower-airway bronchospasm — it does nothing for the laryngeal edema or the shock.
Q3 Put in order
Put the nurse’s first four actions in priority order:
  1. A. Activate the rapid response and notify the provider
  2. B. Stop the antibiotic infusion
  3. C. Give epinephrine IM in the anterolateral thigh
  4. D. Position supine with legs elevated and apply high-flow oxygen
Reveal answer & rationale
Correct order: B → C → D → A
Stopping the infusion (B) takes seconds and cuts off the antigen still feeding the reaction. Epinephrine (C) comes immediately next — it is the intervention that changes survival, and nothing may delay it. Positioning and oxygen (D) support the emptied circulation and the narrowed airways. Then escalate (A). Calling first leaves the patient receiving allergen, unmedicated and upright while you are on the phone; the rapid response arrives to a patient already treated.
Q4 Multiple choice
Thirty minutes later the patient’s BP is 112/70 and she feels "back to normal." She asks to walk to the bathroom. The best response is:
  1. A. Assist her to stand slowly at the bedside before walking
  2. B. Allow ambulation with a staff member at her side
  3. C. Keep her supine with legs elevated and offer a bedpan, explaining that sitting or standing up suddenly is dangerous right now
  4. D. Raise the head of the bed fully so she can adjust before standing
Reveal answer & rationale
Answer: C
She stays supine (C): after anaphylaxis the circulation is still dilated and leak-depleted, and sitting up before she is clearly stabilized risks empty ventricle syndrome, a profound fall in blood pressure that can be fatal (Canadian anaphylaxis review, 2024), and she should not stand or walk even though she feels better (NHS). "Slowly" (A), "supervised" (B), and "head of bed first" (D) all still create the upright shift the guidance warns against — and feeling better does not end the risk, since a biphasic recurrence can strike hours later.
Q5 Select all that apply
Before discharge the patient is prescribed an epinephrine auto-injector. Which teaching points does the nurse include? Select all that apply.
  1. A. Press the tip firmly against the mid outer thigh and hold — through clothing if necessary
  2. B. Get emergency medical care immediately after every injection, even if symptoms improve
  3. C. Carry two auto-injectors at all times
  4. D. Take an oral antihistamine first, and inject epinephrine only if it does not help
  5. E. Return to the ED immediately if symptoms come back hours after this reaction
  6. F. Store the device in the refrigerator to keep the drug potent
Reveal answer & rationale
Answer: A, B, C, E
Correct technique is the mid outer (anterolateral) thigh, held in place, clothing no barrier in an emergency (A). The injection buys time — it never replaces emergency care, so EMS follows every use (B). About 35% of patients need a second dose, so she carries two (C). Biphasic reactions return in up to 20% of cases, peaking 8–11 hours out, with no re-exposure needed (E). Antihistamine-first (D) is the same trap in outpatient form — delay is the killer. Devices are stored at room temperature away from light and heat, never refrigerated (F).

Common questions

What causes anaphylaxis & hypersensitivity reactions?
Common causes and risk factors include foods — peanuts especially; tree nuts, fish, shellfish, milk, eggs, wheat, soy, sesame, red meat (regional patterns: peanut/tree nut in north america–australia, shellfish in asia, sesame in the middle east), insect stings (bee, fire ant venom), medications — with foods and venom, one of the three most frequent trigger groups worldwide (wao), natural rubber latex, radiocontrast media & medical dyes, and others.
What are the early signs of anaphylaxis & hypersensitivity reactions?
Early findings include Generalized urticaria (hives), itching, flushing.
Which findings should a nurse report immediately in anaphylaxis & hypersensitivity reactions?
Report immediately: Generalized urticaria (hives), itching, flushing, Angioedema — swollen lips, tongue, uvula; periorbital edema, Throat tightness, voice change, stridor, Wheeze, cough, dyspnea (respiratory involvement in ~85%), Hypoxemia (falling SpO₂), and others. These signal deterioration that needs rapid intervention.
What are the four types of hypersensitivity reactions?
Type I (immediate): IgE on mast cells, reacting within minutes — anaphylaxis, allergic asthma, urticaria. Type II (cytotoxic): IgG/IgM antibodies destroying antibody-tagged cells — hemolytic transfusion reaction, autoimmune hemolytic anemia. Type III (immune complex): antigen–antibody complexes depositing in skin, joints and kidneys — serum sickness, lupus nephritis. Type IV (delayed): T-cell-mediated with no antibody, appearing 48–72 hours after exposure — contact dermatitis, the PPD skin test. Timing is the fastest way to tell them apart: minutes = I, days = IV.
Why is epinephrine given before antihistamines in anaphylaxis?
Because only epinephrine reverses the mechanism: its alpha-1 vasoconstriction counters the vasodilation and capillary leak while its beta effects open the bronchi. Antihistamines relieve skin symptoms, but their benefit in anaphylaxis itself is unproven, and WAO warns they can delay repeated epinephrine — the intervention that determines survival. With half of fatalities occurring in the first hour and no absolute contraindication to IM epinephrine, nothing comes before it.
What is a biphasic anaphylactic reaction?
A return of symptoms after apparent resolution, without any new exposure. It occurs in up to 20% of cases (clinically significant in 4–5%) and peaks 8–11 hours after the initial reaction — WAO notes about half occur within 6–12 hours. This is why patients are observed at least 4 hours (longer after severe or multiple-dose reactions) and taught to seek emergency care immediately if symptoms come back.

Sources

Reviewed by Hae Suk Lee, RN

Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.

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