New anaphylaxis definitions and management

Professor Peter Smith — new anaphylaxis definitions and management

Allergy and immunology; active member of the Australasian Society of Clinical Immunology and Allergy (ASCIA). Otter/intro name Smith — we keep that byline and do not invent an alternate surname or extra credentials beyond ASCIA / allergy–immunology framing in the lecture.

Host

Healthed seminar host (speaker intro; main talk is Professor Peter Smith).

Why update — Australia’s fatality problem

Australia has one of the highest anaphylaxis rates in the world. We also have some of the best education resources and pioneered standardised guidelines — yet between 1997 and 2013, anaphylaxis fatalities doubled while rates in many other places were slowing.

Only about 1 in 10 fatal cases received adrenaline first. Recognition fails; adrenaline is delayed or omitted; patients stand up after treatment; or there is no ongoing plan. The talk’s through-line is simple: recognise sooner, give adrenaline earlier, keep people lying/sitting with legs up, and close the loop with devices and ASCIA plans before they leave.

New GALEN/GAPA global definition

After about two decades of the NIAID / Food Allergy and Anaphylaxis Network definition, and a 2020 World Allergy Organization (WAO) wording that was not widely benchmarked or adopted, a GALEN subgroup — GAPA (global anaphylaxis and food allergy groups) — rebuilt consensus.

Professor Smith was among 46 global experts (12-person writing team; Delphi consensus requiring strong agreement), engaging 46 patient organisations. The agreed wording:

Clinicians sometimes flinch at putting “death” in a definition. Patient organisations insisted on it so the condition is not taken lightly. Fatality risk among true anaphylaxis episodes is often cited in a wide range (roughly 1 in 100 to 1 in 10,000 depending on context) — many people recover, but death is real enough that the wording matters.

Conditional diagnostic criteria

The logic is conditional: how sure you are about allergen exposure changes how many organ systems you need before you call it anaphylaxis and treat.

1 — No known allergen

Need skin/mucosal involvement plus respiratory or cardiovascular compromise. Gastrointestinal alone with circulatory collapse is not criterion‑1 anaphylaxis — GI is deliberately out of this arm so you do not mislabel other shock syndromes.

2 — Likely allergen

Any two organ systems count, including GI, respiratory, cardiovascular, and skin/mucosal (including oral involvement).

3 — Known allergen

Examples given: peanut, cashew, prawn. In Queensland, the speaker noted more shellfish fatalities than nut fatalities. Isolated cardiovascular compromise/shock or isolated respiratory compromise is enough — do not wait for a rash.

In adults, roughly ~80% present respiratory-predominant and ~20% cardiovascular-predominant. Blood pressure can fall so quickly there is no visible rash.

Adrenaline early — first three choices

The Australian management culture (including ASCIA plans) has long carried the spirit of early adrenaline — the talk referenced a 1990s Director-General quote about “fentanyl adrenaline” / give it early, and guideline language from ~2015 affirming early use.

Practical framing from the lecture: if this is anaphylaxis, the first three choices are adrenaline, adrenaline, adrenaline. Repeat every 5–15 minutes as needed. After a second dose, start thinking about the IV infusion pathway and escalation (ambulance / ED).

Adrenaline remains appropriate in pregnancy when indicated. Needle-free options matter for needle-phobic patients and for earlier self-use — covered under devices below.

Positioning — don’t stand them up

Anaphylaxis vasodilates. Fluid can shift into extravascular compartments — up to about one-third of circulating volume in severe cases. Adrenaline vasoconstricts against that backdrop. If you then stand the patient, sudden postural redistribution can be catastrophic — “unconscious and dead” in the speaker’s blunt framing.

Keep patients lying flat (or sitting if breathing is easier) with legs elevated when appropriate — elevating the legs can return roughly 0.5–1 L of volume. Do not walk them. One fatality anecdote (Richard Humphrey’s series): a patient carried down stairs feet-first after adrenaline — enough positional insult to contribute to death. Carry head-up / careful positioning; never “walk it off.”

Infants and autoinjector thresholds

Infants have roughly three times the surface area per body mass of adults — vasodilation hits blood pressure harder. They often look agitated or floppy rather than verbalising respiratory distress as an early sign.

Drawing up adrenaline by weight (classic 0.01 mg/kg framing) under panic is error-prone in ED, let alone for parents. Australia has moved junior autoinjector thresholds downward over time: historically ~15 kg → ~10 kg → toward ~7.5 kg for junior devices — making correct IM delivery more realistic than vials and broken needles.

Devices, ASCIA plans, nasal neffy

Australia now has multiple adrenaline device options and five ASCIA action plans, including a green plan for patients without an adrenaline device. Guidelines are living documents and align with broader GALEN/GAPA thinking.

• EpiPen — longstanding workforce device in Australia
• Anapen
• Jext
• Anzen (“Azure” pending naming in the talk) — emerging option discussed as pending/available in the device landscape
• Nasal neffy — needle-free (see below)

Nasal neffy (Intravail)

Otter heard “nephew / netting” — clinical product is neffy, using Intravail (also used for years in nasal overdose antidote formulations such as naltrexone contexts). Framed for ≥15 kg and ≥4 years. Real-world US experience approaching about a year at the time of the talk; clinic efficacy data longer.

• Do not prime — priming wastes the single dose (same rule as not “practising” an EpiPen)
• Mucus present is OK — adhesion can still work
• Better high-temperature stability data; shelf life around ~2.5 years
• Needle-free → often carried and used earlier
• Repeat dose: second spray in the nose if needed

IM and IN adrenaline are treated as similarly efficacious in the updated pathway framing; choose what the patient will actually carry and use. High skin-to-muscle distance (body habitus) can complicate IM delivery; ideal autoinjector depth is often discussed around ~12–13 mm into the outer thigh.

Acute pathway and refractory ladder

Adjuncts, observation, biphasic risk

• Steroids — no good evidence they help in the acute phase; no point in a three-day steroid course “for anaphylaxis” as a default from this talk
• Injected antihistamines — no role; may worsen hypotension / precipitate problems — do not inject antihistamines for acute anaphylaxis
• Observe ≥4 hours after treatment
• Biphasic reactions in about 3–20% — more likely if adrenaline was delayed or asthma is poorly controlled; consider overnight observation if refractory, needed IV infusion, lives alone, or lacks ready devices

Anaphylaxis can occur without skin symptoms. Prescribers (including nurse practitioners in the talk’s framing) should keep CPR instructions in mind if the patient becomes unresponsive.

Queensland fatality data and tryptase

Jack Darling’s PhD (speaker supported) looked at local fatalities. Against a common “asthma kills in anaphylaxis” narrative, Queensland data pointed to pre-existing cardiac disease as a major local driver of death — especially medication and idiopathic anaphylaxis on a compromised heart. Asthma remains important (about 28% of the fatality series vs roughly double background adult asthma prevalence), but it is not the whole story. In that ~20-year cohort there were only two paediatric fatalities and 14 food-allergy fatalities — relatively strong compared with national framing.

About 57% of fatality cases had pristine airways at examination in the series discussed — reinforcing that CV collapse without obvious airway catastrophe is still anaphylaxis.

Tryptase

• Usual upper reference ~11.5 µg/L
• Fatal cases: mean tryptase around ~220 µg/L; with asthma, mean around ~150 µg/L
• Process properly: spin down, keep cool — do not leave on the bench to degrade
• A single ED value is incomplete — need a baseline and whether it returns
• Persistently elevated baseline (thinking around >8 µg/L even while “normal” upper is ~11.5) → consider hereditary alpha-tryptasemia (HαT) (described ~2016; extra TPSAB1 copies → amplified allergic responses)

Cofactors that lower the threshold

Shelley Dua’s work (sleep restriction to ~2 hours; exercise to ~85% VO₂ max) showed roughly half the peanut dose could trigger anaphylaxis. Other cofactors from the talk:

• Intercurrent infection, alcohol, stress
• NSAIDs, ACE inhibitors, beta-blockers
• Poorly controlled asthma
• Adolescents not carrying devices
• Advanced age and cardiovascular disease

Monday morning — close the loop

Danish data vignette: among a small series of adolescents/young adults (18–35), 6 of 11 never even picked up their adrenaline device from hospital pharmacy. Enthusiasm of the clinician shapes patient engagement.

1. Prescribe and dispense before they leave the room / suite
2. Demonstrate with a trainer matching the device
3. Print / send the correct ASCIA plan (online)
4. Refer and book follow-up / documentation
5. Know repeat dosing; call ambulance if a second dose is needed and escalation is required

Emerging research (brief)

Take-home messages for clinic

1. Australia’s rates are high and fatalities rose historically while adrenaline-first treatment was rare (~1 in 10 fatal cases).
2. New definition: serious allergic hypersensitivity that can progress rapidly and may cause death.
3. Criteria are conditional — known allergen → isolated CV or respiratory is enough; do not wait for rash.
4. Adrenaline / adrenaline / adrenaline; repeat 5–15 min; after dose two think IV infusion.
5. Never stand patients up after adrenaline; legs up returns volume.
6. Infants: floppy/agitated; junior device toward ~7.5 kg.
7. Match device to training; five ASCIA plans including green; neffy ≥15 kg / ≥4 y — don’t prime.
8. No acute role for steroids or injected antihistamines; observe ≥4 h; biphasic 3–20%.
9. QLD: cardiac disease is a major fatality driver; process tryptase and get baselines; think HαT if persistently elevated.
10. Monday: prescribe + dispense + trainer + ASCIA plan + follow-up before they leave.

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