Allergic Reactions and Anaphylaxis - NREMT AEMT Level

SECTION 1

Historical Context & Motivation

The phenomenon of exaggerated immune responses to otherwise harmless substances has been documented for millennia, though systematic understanding only emerged in the late nineteenth and early twentieth centuries. Ancient Egyptian records describe the death of Pharaoh Menes around 2641 BCE, allegedly from a wasp sting—possibly the first recorded case of anaphylaxis. The term "allergy" itself was not coined until 1906, when Viennese pediatrician Clemens von Pirquet observed that some patients reacted to serum therapy in a manner opposite to the intended protective response. These observations laid the groundwork for immunology as a discipline and, critically, for the prehospital emergency protocols that Advanced Emergency Medical Technicians (AEMTs) rely on today. Understanding the historical evolution of allergy science helps contextualize why rapid field identification of allergic reactions and anaphylaxis remains one of the most time-sensitive interventions in the AEMT scope of practice.

1902 • Discovery of Anaphylaxis

Charles Richet and Paul Portier demonstrated that re-exposure to sea anemone toxin in dogs produced a fatal hypersensitivity reaction, coining the term anaphylaxis (meaning "against protection"). Richet later received the Nobel Prize in 1913 for this work.

1906 • "Allergy" Defined

Clemens von Pirquet introduced the term "allergy" to describe altered immune reactivity, distinguishing beneficial immunity from harmful hypersensitivity.

1963 • Gell–Coombs Classification

Philip Gell and Robin Coombs published their classification of four types of hypersensitivity reactions. Type I (immediate) became the framework for understanding anaphylaxis.

1977 • Epinephrine Auto-Injectors

The first epinephrine auto-injector (EpiPen) was developed by Sheldon Kaplan, enabling rapid prehospital treatment of anaphylaxis by trained providers and patients.

2020 • WAO Updated Guidelines

The World Allergy Organization updated international anaphylaxis guidelines, emphasizing intramuscular epinephrine as the first-line treatment and establishing standardized clinical criteria for prehospital diagnosis.

Despite these advances, anaphylaxis continues to cause preventable deaths in and out of hospital settings, primarily because of delayed recognition and treatment. The central question for every AEMT remains: how do you rapidly differentiate a localized allergic reaction from a systemic, life-threatening anaphylactic event, and what interventions must be initiated immediately in the field to prevent cardiovascular collapse and airway compromise?

SECTION 2

Core Principles & Definitions

At the molecular level, an allergic reaction represents a misdirected immune response in which the body's defenses attack a typically harmless substance known as an allergen. The process begins with an initial exposure that primes the immune system—a phase called sensitization—during which allergen-specific immunoglobulin E (IgE) antibodies are produced and attach to the surface of mast cells and basophils. Upon subsequent re-exposure, the allergen cross-links these surface-bound IgE molecules, triggering rapid degranulation—a massive release of chemical mediators including histamine, leukotrienes, and prostaglandins. These mediators produce the clinical signs AEMTs must recognize: vasodilation, increased vascular permeability, bronchoconstriction, and mucous hypersecretion.

Allergen & Sensitization

An allergen is any substance that provokes an immune-mediated hypersensitivity reaction. Common allergens include insect venoms, foods (peanuts, shellfish), medications (penicillin, NSAIDs), and latex. Sensitization occurs during initial exposure, producing allergen-specific IgE.

Mast Cell Degranulation

Upon re-exposure, allergen cross-links IgE on mast cell surfaces, triggering degranulation. Preformed granules release histamine within seconds. Newly synthesized mediators (leukotrienes, prostaglandins) follow within minutes, sustaining and amplifying the reaction.

Localized vs. Systemic Reactions

Localized reactions affect a single organ system—urticaria (hives), rhinitis, or local edema. Systemic anaphylaxis involves two or more organ systems simultaneously and can progress to cardiovascular collapse within minutes if untreated.

Anaphylaxis Criteria

Anaphylaxis is diagnosed clinically when there is acute onset of illness with involvement of skin/mucosal tissue PLUS respiratory compromise OR hypotension, OR acute onset after exposure to a known allergen with rapid hypotension (systolic BP < 90 mmHg or > 30% decrease from baseline).

Biphasic Reactions

Up to 20% of anaphylaxis episodes feature a biphasic pattern in which symptoms recur 1–72 hours (typically 8–12 hours) after initial resolution. This mandates extended observation and hospital transport even when field treatment is successful.

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KEY TAKEAWAY

Think of sensitization like loading a spring-loaded mousetrap: the first exposure sets the trap (IgE binds to mast cells), and nothing visible happens. The second exposure is the mouse stepping on the trigger—sudden, explosive mediator release occurs. An AEMT arriving on scene is seeing the trap snap; your job is to neutralize the cascade before the entire house (cardiovascular system) collapses.

SECTION 3

Visual Explanation — The Anaphylaxis Cascade

The diagram above illustrates the sequential cascade from sensitization through clinical manifestation. Note the four affected organ systems—cardiovascular, respiratory, integumentary, and gastrointestinal—and the diagnostic threshold for anaphylaxis shown in the dashed-border alert box.

The cascade depicted above underscores the speed and systemic nature of anaphylaxis. From the moment an allergen cross-links IgE on mast cell surfaces, the pathophysiological clock begins ticking in seconds rather than minutes. Histamine acts almost instantaneously on H₁ and H₂ receptors throughout the body, producing vasodilation in the peripheral vasculature, bronchoconstriction in the lower airways, and increased capillary permeability that allows plasma to shift from the intravascular compartment into interstitial spaces. This plasma shift is what produces both the visible swelling (angioedema) and the critically dangerous distributive shock—relative hypovolemia despite no actual blood loss. As an AEMT, you should internalize that any combination of two or more organ system involvement following known or suspected allergen exposure constitutes anaphylaxis and demands immediate epinephrine administration.

SECTION 4

Pharmacological Mechanism — Epinephrine & Adjunct Therapies

Epinephrine is the cornerstone of anaphylaxis treatment because it directly opposes every major pathophysiological mechanism of the reaction. Its pharmacological action is mediated through adrenergic receptor subtypes, and understanding these receptors explains why no other single medication can replace it in the acute setting. At the AEMT level, you are authorized to administer epinephrine via intramuscular injection and, depending on local protocol, to assist with auto-injector use for patients who carry their own devices.

Adrenergic Receptor Actions of Epinephrine

Receptor	Location	Epinephrine Effect	Clinical Benefit
Alpha-1 (α₁)	Peripheral vasculature	Vasoconstriction	↑ SVR, ↑ BP, ↓ mucosal edema, ↓ urticaria
Beta-1 (β₁)	Myocardium	↑ Heart rate, ↑ contractility	↑ Cardiac output to counteract shock
Beta-2 (β₂)	Bronchial smooth muscle	Bronchodilation	Reverses bronchoconstriction, ↓ wheezing
Beta-2 (β₂)	Mast cells	↑ cAMP → inhibits degranulation	Slows further mediator release

Adrenergic receptor effects of epinephrine relevant to anaphylaxis management

AEMT Dosing Protocols

ADULT EPINEPHRINE DOSE

Epinephrine 1:1,000 (1 mg/mL) → 0.3 − 0.5 mg IM (lateral thigh)

Concentration: 1 mg per 1 mL. Route: intramuscular into the vastus lateralis. May repeat every 5−15 minutes if symptoms persist. The 1:1,000 concentration is used for IM injection; never confuse with IV concentration (1:10,000).

PEDIATRIC EPINEPHRINE DOSE

0.01 mg/kg IM (max 0.3 mg per dose)

For a 20 kg child: 0.01 × 20 = 0.2 mg IM. Always use weight-based dosing for pediatric patients. Auto-injector doses: EpiPen Jr = 0.15 mg (15−30 kg), EpiPen = 0.3 mg (≥ 30 kg).

Adjunct Medications

While epinephrine remains the only first-line agent, several adjunct medications may be administered within the AEMT scope of practice (protocol-dependent). Diphenhydramine (Benadryl, 25–50 mg IV/IM) is an H₁-receptor antagonist that reduces urticaria and pruritus but does not reverse bronchospasm or hypotension and should never delay epinephrine. Albuterol (2.5 mg nebulized) serves as a β₂-selective bronchodilator for persistent wheezing after epinephrine. Normal saline bolus (1–2 L for adults) addresses hypovolemia from third-spacing. Critically, none of these adjuncts replace epinephrine—they are supportive measures only.

SECTION 5

Detailed Assessment & Classification

Accurate field assessment is the bridge between pathophysiology knowledge and life-saving intervention. The AEMT must systematically evaluate the patient using a structured approach that integrates history of present illness, physical examination findings, and vital sign trends. The severity classification system below guides treatment decisions and transport priority, helping you communicate clearly with receiving facilities and medical direction.

This diagram presents the severity spectrum from mild localized reactions through moderate to severe anaphylaxis, paired with a decision flowchart that mirrors the structured assessment approach an AEMT should follow on scene. Note that the decision point hinges on the anaphylaxis diagnostic criteria—any delay in recognizing this threshold directly impacts patient outcomes.

SAMPLE & OPQRST in Allergic Reactions

During the focused history, utilize the SAMPLE mnemonic to gather critical data: Signs/Symptoms (onset, progression, and organ systems involved), Allergies (the specific trigger, prior reaction severity, and history of anaphylaxis), Medications (current prescriptions, especially beta-blockers which can make anaphylaxis refractory to epinephrine), Past medical history (asthma, atopy, prior anaphylaxis), Last oral intake (relevant if food-triggered), and Events leading to the present illness. Supplement this with OPQRST to characterize any associated pain or discomfort. Pay particular attention to patients on beta-blockers, as these medications blunt the compensatory tachycardia response and may render standard epinephrine doses less effective, potentially necessitating glucagon administration at the hospital level.

SECTION 6

Worked Example — Prehospital Anaphylaxis Management

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SCENARIO

You are dispatched to a local restaurant for a 34-year-old female with difficulty breathing. Upon arrival, the patient is sitting upright, appears anxious, and has diffuse hives across her trunk and arms. She states she ate shrimp 15 minutes ago and "felt her throat closing." She has a known shellfish allergy and carries an EpiPen but did not use it. Her friend reports the patient's lips are swollen and she has been "wheezy" since symptoms started.

Systematic AEMT Anaphylaxis Management

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Step 1 — Scene Safety & General Impression

Ensure scene safety and don appropriate PPE. On approach, your general impression reveals a patient in acute distress: sitting tripod position, audible wheezing, visible facial edema, and diffuse urticaria. This presentation immediately raises concern for anaphylaxis.

Priority: Emergent — multi-system allergic reaction suspected.
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Step 2 — Primary Survey (ABCDE)

Airway: Patent but patient reports throat tightness; no stridor yet audible. Angioedema of lips noted. Breathing: RR 28, bilateral expiratory wheezing, SpO₂ 91% on room air, using accessory muscles. Circulation: HR 118, BP 88/52, skin warm and flushed with generalized urticaria. Disability: Alert, anxious, GCS 15. Exposure: Generalized hives on trunk and extremities; no rash on palms/soles.

Anaphylaxis criteria MET: Skin involvement (urticaria, angioedema) + Respiratory compromise (wheezing, SpO₂ 91%) + Hypotension (SBP 88).
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Step 3 — Immediate Interventions

Administer epinephrine 0.3 mg IM (1:1,000) into the lateral thigh (vastus lateralis) immediately. Apply high-flow O₂ via non-rebreather mask at 15 LPM. Position patient supine with legs elevated (Trendelenburg) to support venous return—if respiratory distress is severe, a semi-Fowler's position may be more appropriate. Establish IV access with a large-bore catheter (18G or larger) and initiate a 1 L normal saline bolus to address distributive hypovolemia.

Epi 0.3 mg IM given at T+0 min | O₂ 15 LPM NRB | IV NS wide open
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Step 4 — SAMPLE History & Reassessment

While partner drives, obtain SAMPLE: S—hives, dyspnea, throat tightness, nausea; A—shellfish (known severe); M—oral contraceptive only (no beta-blockers); P—prior anaphylaxis to shellfish 2 years ago; L—shrimp meal 15 minutes ago; E—symptoms began 10 minutes after eating. Reassess at 5 minutes: HR 110, BP 94/60 (improving), SpO₂ 94%, wheezing diminishing. Document epinephrine administration time and response.

Partial improvement at 5 min. Continue monitoring; be prepared to repeat epi in 5−15 min if symptoms plateau or worsen.
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Step 5 — Adjunct Therapy & Transport

Per local protocol, administer diphenhydramine 50 mg IV/IM and consider nebulized albuterol 2.5 mg for persistent wheezing. Continue NS bolus. Provide early notification to the receiving ED with a structured report: "34F anaphylaxis secondary to shellfish ingestion, epinephrine 0.3 mg IM administered at [time], partial improvement, en route." Reassess every 5 minutes during transport. At 10 minutes post-epi: HR 100, BP 102/68, SpO₂ 97%, wheezing resolved, hives fading.

Good response to single dose epinephrine. Transport to ED for observation (biphasic risk). No repeat dose needed.

SECTION 7

Common Allergen Categories & Differential Diagnosis

A thorough understanding of common allergen categories helps the AEMT anticipate the severity and progression of reactions. Additionally, several conditions mimic anaphylaxis and must be considered during differential diagnosis to avoid both under-treatment and over-treatment. The tables below organize this information for rapid clinical reference.

Allergen Category	Common Examples	Typical Route	Onset Speed	Severity Risk
Insect Venoms	Bee, wasp, hornet, fire ant	Injection (sting)	5−15 minutes	High — rapid systemic spread
Foods	Peanuts, tree nuts, shellfish, eggs, milk	Ingestion	5−30 minutes	High — most common cause of fatal anaphylaxis
Medications	Penicillin, sulfa drugs, NSAIDs, aspirin	Oral / IV / IM	Seconds (IV) to 30 min (oral)	Very high for IV medications
Latex	Gloves, catheters, balloons	Contact / mucosal	Minutes to hours	Moderate — healthcare workers at increased risk
Environmental	Pollen, mold, animal dander, dust mites	Inhalation	Minutes	Low — typically localized (rhinitis, asthma)

Common allergen categories encountered in prehospital settings

Differential Diagnosis: Conditions That Mimic Anaphylaxis

Condition	Key Differentiating Features
Vasovagal syncope	Bradycardia (not tachycardia), pallor (not flushing), no urticaria, rapid recovery when supine
Asthma exacerbation	Isolated bronchospasm without skin findings, hypotension, or GI symptoms; history of asthma
Panic / anxiety attack	Hyperventilation, tingling extremities, no urticaria or hypotension, normal SpO₂
Angioedema (ACE-inhibitor)	Facial/tongue swelling without urticaria; bradykinin-mediated (not histamine); does NOT respond to epinephrine
Septic shock	Hypotension and tachycardia present, but gradual onset over hours with fever; no urticaria

Differential diagnosis for conditions mimicking anaphylaxis

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KEY TAKEAWAY

When in doubt, err on the side of treating for anaphylaxis. The risk of withholding epinephrine from a true anaphylaxis patient (potential death) far outweighs the risk of administering it to a patient who turns out to have a milder condition (transient tachycardia, pallor). This risk-benefit calculus is analogous to the decision to defibrillate a pulseless patient—the cost of inaction is catastrophic, while the cost of action is manageable.

SECTION 8

Connection to Advanced Theory — Anaphylactoid Reactions & Paramedic-Level Care

As AEMTs progress toward paramedic-level practice, several advanced concepts expand on the foundational knowledge of allergic reactions and anaphylaxis. Understanding these concepts now strengthens clinical reasoning and prepares you for expanded scope interventions. The distinction between true anaphylaxis and anaphylactoid reactions is clinically significant: anaphylactoid reactions produce identical signs and symptoms but occur without prior sensitization and are not IgE-mediated. Radiocontrast media, opioids, and vancomycin can trigger direct mast cell degranulation on first exposure, bypassing the sensitization phase entirely. Despite the different mechanism, prehospital treatment is identical—epinephrine remains the first-line intervention because the downstream pathophysiology is the same.

Feature	AEMT Scope	Paramedic Scope
Epinephrine Route	IM only (auto-injector or ampule)	IM and IV push / IV infusion (1:10,000 for IV)
Airway Management	BLS airway adjuncts, supraglottic devices	Rapid sequence intubation, surgical cricothyrotomy
Vasopressors	Not in scope	Epinephrine drip, norepinephrine, vasopressin for refractory shock
Corticosteroids	Generally not in scope	Methylprednisolone / dexamethasone IV for biphasic prevention
Glucagon	Not in scope	1−5 mg IV for beta-blocker-refractory anaphylaxis
Cardiac Monitoring	Pulse oximetry, vital signs	12-lead ECG, continuous cardiac monitoring, capnography

AEMT vs. Paramedic scope comparison for anaphylaxis management

It is also important for the AEMT to understand the concept of refractory anaphylaxis—cases in which the patient fails to respond to repeated IM epinephrine doses. Risk factors include delayed treatment, concurrent beta-blocker use, massive allergen exposure, and mast cell disorders such as mastocytosis. When you encounter a patient who does not improve after two IM epinephrine doses, communicate this urgently to medical direction and the receiving facility, as these patients will likely require IV epinephrine infusion and advanced airway management. Your early recognition and clear communication can save critical minutes in the chain of care.

SECTION 9

Practice Problems

Question 1: CONCEPTUAL

Explain why a patient's first exposure to an allergen does not produce an anaphylactic reaction, but a subsequent exposure can be life-threatening. In your explanation, identify the role of IgE, mast cells, and the process of sensitization.

Show answer

During the initial exposure, the immune system identifies the allergen and produces allergen-specific IgE antibodies through a process called sensitization. These IgE molecules bind to high-affinity FcεRI receptors on the surface of mast cells and basophils, effectively "arming" them. No significant clinical reaction occurs because the mast cells have not yet been triggered. Upon subsequent re-exposure, the allergen cross-links the surface-bound IgE molecules, which signals the mast cells to degranulate—releasing a massive bolus of preformed mediators including histamine, as well as newly synthesized leukotrienes and prostaglandins. This cascading release produces the multi-system effects of anaphylaxis: vasodilation, bronchoconstriction, increased vascular permeability, and mucous hypersecretion.

Question 2: BASIC CALCULATION

A 22 kg pediatric patient is experiencing anaphylaxis. Calculate the appropriate epinephrine dose using 1:1,000 concentration (1 mg/mL). What volume in milliliters would you draw up?

Show answer

Using the pediatric dosing formula: 0.01 mg/kg × 22 kg = 0.22 mg. Since the 1:1,000 epinephrine concentration provides 1 mg per 1 mL, the volume to administer is 0.22 mL IM into the lateral thigh. This dose falls within the acceptable range (maximum 0.3 mg per dose for pediatric patients). If using an auto-injector, the EpiPen Jr (0.15 mg) would be appropriate for patients 15−30 kg, but the calculated dose of 0.22 mg is higher than the auto-injector delivers, so drawing from a vial is preferred when available and within protocol.

Question 3: INTERMEDIATE

You respond to a call for a 58-year-old male with generalized hives and difficulty breathing after a bee sting. His medications include metoprolol (a beta-blocker) and lisinopril (an ACE inhibitor). His vital signs are: HR 72, BP 76/48, RR 26, SpO₂ 89%. You administer epinephrine 0.3 mg IM. After 5 minutes, his HR is 76, BP 78/50, and SpO₂ 90%. Why might this patient be responding poorly to epinephrine, and what should your next steps be?

Show answer

This patient's poor response to epinephrine is likely due to his beta-blocker (metoprolol). Beta-blockers competitively occupy beta-adrenergic receptors, blocking epinephrine's β₁ effects (increased heart rate and contractility) and β₂ effects (bronchodilation). This explains why his heart rate remained relatively low (72→76) despite severe hypotension, as the normal compensatory tachycardia is being pharmacologically blunted. Your next steps should include: (1) Repeat epinephrine 0.3−0.5 mg IM; (2) Continue aggressive IV fluid resuscitation with normal saline; (3) Contact medical direction to report refractory anaphylaxis in a beta-blocker-dependent patient; (4) Anticipate the need for glucagon at the receiving facility, which bypasses beta receptors to increase cardiac output via cAMP; (5) Maintain high-flow O₂ and consider nebulized albuterol for persistent bronchospasm; (6) Rapid transport with early hospital notification.

Question 4: APPLIED

You arrive at a daycare where a 4-year-old (weight ~16 kg) accidentally ate a cookie containing peanuts. The child has hives on the face and trunk, lip swelling, is crying but breathing without stridor or wheezing, HR 130, BP 90/60, SpO₂ 96%. The daycare has an EpiPen Jr (0.15 mg) prescribed for the child. Does this child meet anaphylaxis criteria? Describe your complete management plan including medication dosing, oxygen administration, IV access, and transport decisions.

Show answer

This child demonstrates skin involvement (generalized urticaria, lip angioedema) following known allergen exposure, but currently has stable respiratory status (no stridor, no wheezing, SpO₂ 96%) and borderline blood pressure. The tachycardia (HR 130) is concerning but may reflect anxiety in a 4-year-old. Strictly applying diagnostic criteria, anaphylaxis requires skin involvement PLUS respiratory compromise or hypotension—this child is at the threshold and allergic reactions can rapidly progress, especially with food allergens. Given the known severe peanut allergy, visible angioedema, and potential for rapid deterioration, the prudent AEMT action is to administer the prescribed EpiPen Jr (0.15 mg IM, lateral thigh). Calculated dose: 0.01 mg/kg × 16 kg = 0.16 mg, confirming the auto-injector dose is appropriate. Apply blow-by or mask O₂ as tolerated, establish IV access (may be challenging in a distressed child—do not delay transport), prepare NS bolus if hypotension develops, and transport with continuous reassessment every 5 minutes. Monitor for biphasic reaction potential and communicate early with the pediatric receiving facility.

Question 5: CRITICAL THINKING

A 42-year-old female presents with acute facial and tongue swelling, difficulty swallowing, and mild hoarseness that began 2 hours ago without any known allergen exposure. She denies itching or hives. Her medications include lisinopril (ACE inhibitor) started 3 weeks ago. Vital signs: HR 82, BP 138/88, RR 20, SpO₂ 95%. Compare and contrast this presentation with true anaphylaxis. Would you administer epinephrine? Defend your clinical reasoning.

Show answer

This presentation is most consistent with ACE-inhibitor-induced angioedema (bradykinin-mediated) rather than true IgE-mediated anaphylaxis, based on several distinguishing features. First, the absence of urticaria (hives) and pruritus argues strongly against histamine-mediated anaphylaxis, as skin findings are present in approximately 90% of anaphylaxis cases. Second, the isolated angioedema without respiratory distress (wheezing/bronchospasm), cardiovascular compromise (hypotension/tachycardia), or GI symptoms suggests a single-organ, non-IgE mechanism. Third, the temporal relationship to lisinopril initiation (3 weeks) fits the classic timeline for ACE-inhibitor angioedema, which can occur days to years after starting therapy. Fourth, the patient's blood pressure is elevated (not hypotensive), and heart rate is normal—both atypical for anaphylaxis. However, the clinical decision regarding epinephrine is nuanced. Epinephrine will likely be ineffective because ACE-inhibitor angioedema is bradykinin-mediated, not histamine-mediated, and epinephrine's mechanism targets histamine-pathway effects. That said, if the patient develops airway compromise (stridor, inability to manage secretions), epinephrine may provide marginal benefit through alpha-mediated vasoconstriction to reduce mucosal edema. The appropriate management includes: high-flow O₂, upright positioning, rapid transport to ED for potential icatibant or C1-esterase inhibitor therapy (hospital-only agents), continuous airway monitoring, and having advanced airway equipment immediately accessible. Contact medical direction for guidance on a case that sits in the gray zone between protocols.

SUMMARY

Summary — Allergic Reactions and Anaphylaxis

Summary

Allergic reactions represent a spectrum of immune-mediated responses ranging from localized urticaria and pruritus to life-threatening anaphylaxis. The underlying mechanism involves IgE-mediated sensitization during initial allergen exposure, followed by explosive mast cell degranulation upon re-exposure, releasing histamine, leukotrienes, and prostaglandins that produce vasodilation, bronchoconstriction, increased vascular permeability, and distributive shock. Anaphylaxis is diagnosed clinically by the presence of two or more organ systems involved after known or suspected allergen exposure, particularly the combination of skin/mucosal findings with respiratory compromise or hypotension.

For the AEMT, the definitive first-line treatment is intramuscular epinephrine (0.3−0.5 mg for adults, 0.01 mg/kg for pediatrics) administered into the vastus lateralis (lateral thigh). Epinephrine's alpha-1, beta-1, and beta-2 receptor actions counteract every major pathway of the anaphylactic cascade. Adjunct therapies including diphenhydramine, albuterol, oxygen, and IV normal saline support but never replace epinephrine. Patients on beta-blockers may exhibit refractory anaphylaxis. All patients receiving prehospital anaphylaxis treatment require hospital transport for observation due to the risk of biphasic reactions occurring up to 72 hours after the initial event.