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Anaphylaxis in the Emergency Department

Anaphylaxis is the quintessential medical emergency. It’s sudden, terrifying for the patient and demands rapid, decisive action. As an emergency physician, you are the critical link between a catastrophic outcome and a full recovery.

While the core treatment—intramuscular (IM) adrenaline—is well-known, the nuances of diagnosis, refractory management, and post-emergency care have evolved significantly.

Part 1: Recognition (Is this really anaphylaxis?)

The first hurdle is recognition. Anaphylaxis is not just a bad rash. It is a severe, life-threatening, generalized or systemic hypersensitivity reaction.

The diagnosis is clinical.

  1. Sudden onset.
  2. Rapid progression of symptoms.
  3. Systemic involvement, specifically life-threatening Airway, Breathing, or Circulation problems.

Skin or mucosal changes (urticaria, flushing, angioedema) are present in over 80% of cases and are a helpful clue, but—and this is a critical point—up to 20% of anaphylactic reactions, especially the most severe, have no skin signs. Hypotension may be the only presenting feature.

Key Differential Diagnoses to Consider:

  • Simple Urticaria/Angioedema: No A, B, or C compromise.
  • Severe Asthma Attack: Primarily wheeze, but typically lacks the hypotension, angioedema or cutaneous features. (Crucially, patients with asthma are at higher risk of fatal anaphylaxis).
  • Vasovagal Syncope (Faint): Often follows a trigger (e.g., needle). Presents with bradycardia and pallor, not tachycardia and flushing. Symptoms resolve on lying flat.
  • Panic Attack: Can present with tachypnoea and a sense of “throat closing” but objective signs (hypoxia, hypotension, stridor, wheeze) are absent.
  • Scombroid Poisoning: Histamine toxicity from spoiled fish. Mimics anaphylaxis but is not a true allergy.
  • Hereditary Angioedema: Bradykinin-mediated. Presents with angioedema (often laryngeal) but no urticaria or hypotension. It is critically unresponsive to adrenaline, antihistamines, or steroids.

If a patient has sudden-onset A, B, or C problems after a potential trigger, treat it as anaphylaxis, even if there is no rash.

Part 2: The First 5 Minutes (Resus Room Management)

This is the ABCDE approach. It must be slick and immediate.

1. Call for Help

This is a true emergency. Announce it. Get senior ED help, an anesthetist and experienced nursing staff.

2. A (Airway) & B (Breathing)

  • Look for: Airway swelling (angioedema), stridor, hoarse voice.
  • Look for: Increased work of breathing, wheeze, hypoxia (SpO2 < 94%), fatigue, or confusion (often a pre-terminal sign of hypoxia/hypercapnia).
  • Action:
    • Administer high-flow oxygen (15L via a non-rebreather mask).
    • Secure the airway early if there is any doubt. Laryngeal oedema can make intubation impossible within minutes. Have difficult airway equipment and surgical airway options ready.

3. C (Circulation)

  • Look for: Pale, clammy skin, tachycardia, and hypotension (systolic BP < 90 mmHg or a significant drop from their baseline). Note: A reflex bradycardia (Bezold-Jarisch reflex) can occasionally occur but is rare.
  • Action:
    • Secure large-bore IV access (e.g., 2 x 16G cannulas).
    • Lay the patient flat. If they are hypotensive, elevate their legs. This is a critical, life-saving manoeuvre.
    • WARNING: Do NOT allow the patient to suddenly sit or stand up. This can cause a catastrophic drop in venous return (“empty ventricle syndrome”) and lead to cardiac arrest. If they are vomiting or have severe respiratory distress, a semi-recumbent position is a compromise, but supine is preferred for hypotension.
    • If pregnant, tilt 15 degrees to the left lateral position.

4. The Critical Intervention: Adrenaline (Epinephrine)

This is the single most important drug. It is life-saving. It treats all aspects of the reaction (vasoconstriction for hypotension, bronchodilation, reduced edema and mast cell stabilisation).

  • Drug: Adrenaline 1:1000 (this is the 1 mg/mL ampoule)
  • Dose:
    • Adult & Child >12 years: 500 micrograms (0.5 mL)
  • Route: Intramuscular (IM). Not subcutaneous (absorption is too slow).
  • Site: Anterolateral aspect of the middle third of the thigh. This site provides the most reliable absorption.
  • Repeat: Repeat the dose in 5 minutes if the patient is not improving. There is no maximum number of IM doses; continue every 5 minutes while escalating care.

5. Fluids, Fluids, Fluids

Anaphylaxis is a form of distributive shock. Massive vasodilation and capillary leak can “empty” the intravascular space.

  • Action: Start an immediate IV fluid bolus with a crystalloid (e.g., 0.9% Saline or Hartmann’s).
  • Dose:
    • Adult: 500 – 1000 mL stat.
  • Be prepared to give litres of fluid rapidly.

Part 3: The Adjuncts (What Not to Do First)

This is a major update from older guidelines.

Antihistamines and steroids are no longer recommended for initial emergency treatment.

They do not treat the life-threatening A, B, or C problems. Giving them must not delay adrenaline or fluids.

  • Antihistamines (e.g., Cetirizine, Chlorphenamine):
    • Role: RCUK considers them third-line. They may be given after the patient is stabilised to help with cutaneous symptoms (itch, rash).
    • Why not first? They do nothing for airway obstruction, bronchospasm or hypotension. Sedating H1-blockers (like chlorpheniramine) can cause sedation and hypotension, confusing the clinical picture.
  • Corticosteroids (e.g., Hydrocortisone):
    • Role: No longer routinely advised. Their onset of action is hours, not minutes.
    • Why not first? They do not save lives in the acute phase. The evidence that they prevent biphasic reactions is weak. They may be considered after initial resuscitation for refractory reactions or known severe asthma.
  • Bronchodilators (e.g., Salbutamol):
    • Role: Useful for persistent wheeze after IM adrenaline has been given. Adrenaline is the primary bronchodilator for anaphylaxis; salbutamol is an adjunct.

Part 4: Refractory Anaphylaxis

What if you’ve given 2-3 doses of IM adrenaline and large fluid boluses, but the patient remains hypotensive or hypoxic? This is refractory anaphylaxis.

1. GET EXPERT HELP. NOW!!

This is an immediate call to Anesthetics and ICU. This patient needs central access, arterial monitoring, and vasopressor infusions.

2. Keep Giving IM Adrenaline

Continue IM doses every 5 minutes until IV access and an infusion are established.

3. Adrenaline IV Infusion

This is the definitive treatment for refractory hypotension.

  • Warning: IV bolus adrenaline is dangerous (can cause lethal arrhythmias or hypertensive crisis) and should be reserved for peri-arrest situations by experienced specialists. An infusion is the preferred method.
  • RCUK Peripheral Infusion: This can be started via a large-bore peripheral cannula while awaiting central access.
    • Preparation: Add 1 mg of adrenaline (1mL of 1:1000) to 100 mL of 0.9% sodium chloride. This gives a concentration of 10 micrograms/mL.
    • Administration: Run via a dedicated infusion pump.
    • Dose (Adult & Pediatric): Start at 0.5 – 1.0 mL/kg/hour and titrate to response (e.g., a 70kg adult would start at 35-70 mL/hr) to a target MAP.

4. Second-Line Vasopressors

If the patient is adrenaline-resistant, consider adding a second agent (under specialist guidance):

  • Noradrenaline: Particularly useful for its potent alpha-agonist (vasoconstrictor) effects.
  • Vasopressin: Acts on a different receptor (V1) and is useful in severe vasodilatory shock.

5. The Beta-Blocker Problem

  • The Problem: Patients on beta-blockers (e.g., bisoprolol) may have severe, adrenaline-resistant hypotension and paradoxical bradycardia. Their beta-receptors are blocked, rendering adrenaline’s inotropic and chronotropic effects useless.
  • The Antidote: Glucagon
    • Mechanism: Glucagon activates its own cardiac receptors, which (like beta-receptors) activate adenylyl cyclase and increase intracellular cAMP. This bypasses the blocked beta-receptor and provides the needed inotropic and chronotropic support.
    • Dose: 1-2 mg IV bolus given slowly (over 5 minutes, as it causes vomiting), followed by an infusion of 5-15 micrograms/min if effective.
    • Caveat: Ensure the patient’s airway is protected, as vomiting is very common.

Part 5: Investigations & Discharge Planning

Investigations: Mast Cell Tryptase

This is the key investigation to confirm the diagnosis after the event. It is often done incorrectly.

  • Why? Mast cells release tryptase (along with histamine) during degranulation. Tryptase has a longer half-life (around 2 hours) than histamine (minutes).
  • NICE Guideline Timing:
    1. Sample 1 (Acute): As soon as possible after emergency treatment starts.
    2. Sample 2 (Peak): 1-2 hours after the onset of symptoms (no later than 4 hours).
    3. Sample 3 (Baseline): A convalescent sample taken >24 hours later, or in the outpatient allergy clinic.
  • Interpretation: A diagnosis is supported if the acute (Sample 1 or 2) level is significantly higher than the baseline (Sample 3).

Observation and Discharge

  • Observation Period: All patients should be observed for a minimum of 6 to 12 hours from the onset of symptoms. This is to monitor for a biphasic reaction—a recurrence of symptoms hours later without re-exposure. The observation period should be longer (e.g., 12 hours) for severe, protracted, or refractory reactions.
  • Discharge “Package” (per NICE CG134):
    1. Specialist Referral: Every patient with suspected anaphylaxis must be referred to a specialist allergy clinic for formal diagnosis and management planning.
    2. Adrenaline Auto-Injectors (AAIs): Prescribe AAIs as an interim measure before the specialist appointment if the reaction involved A, B, or C compromise and was likely triggered by a non-avoidable trigger (e.g., food, insect sting) or an unknown trigger.
    3. Prescribe TWO AAIs: NICE guidance is clear on this. Patients should carry two at all times.
    4. Training: You or a trained nurse must train the patient (and family/carers) how to use the specific AAI device you have prescribed using a trainer device.
    5. Action Plan: Provide a written emergency action plan.
    6. Avoidance: Give clear advice on avoiding any known or suspected trigger.

Key Take-Home Messages

  1. Recognise: Sudden onset A, B, or C compromise. Skin signs may be absent.
  2. Position: Lie the patient flat, legs up. Do not let them stand.
  3. Adrenaline: 500mcg (0.5mL) of 1:1000 IM into the thigh.
  4. Repeat: Every 5 minutes if no improvement.
  5. Fluids: Give large-volume crystalloid boluses for hypotension.
  6. Adjuncts: Steroids and antihistamines are NOT a priority. They do not save lives.
  7. Refractory: Get expert help. Start an IV adrenaline infusion (1mg in 100mL) and consider glucagon if the patient is on beta-blockers.
  8. Discharge: Observe 6-12 hours, refer to allergy, and prescribe two AAIs with full training.

References and Further Reading

Primary References (The Core Guidelines)

  1. Resuscitation Council UK (RCUK). (2021). Emergency treatment of anaphylaxis: Guidelines for healthcare providers. Link: https://www.resus.org.uk/library/additional-guidance/guidance-anaphylaxis/emergency-treatment
  2. NICE Guideline [CG134]. (2011, last updated 2020). Anaphylaxis: assessment and referral after emergency treatment. Link: https://www.nice.org.uk/guidance/cg134
  3. European Academy of Allergy and Clinical Immunology (EAACI). (2021). EAACI guidelines: Anaphylaxis (2021 update). Link: https://onlinelibrary.wiley.com/doi/10.1111/all.14920

Further Reading (Consultant-Level & Deep Dives)

  1. Resuscitation Council UK (RCUK). (2021). Refractory anaphylaxis algorithm. Link (PDF): https://www.resus.org.uk/sites/default/files/2021-04/Refractory%20anaphylaxis%20algorithm%202021.pdf
  2. Life in the Fastlane (LITFL).Glucagon as an Antidote. Link: https://litfl.com/glucagon-as-an-antidote/
  3. EMCrit Project.The IBCC chapter on Anaphylaxis. Link: https://emcrit.org/ibcc/anaphylaxis/
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