ICU · resuscitation

Acute Severe Anaphylaxis — Comprehensive Peri-Arrest Management

Also known as Anaphylaxis · Anaphylactic shock · Severe allergic reaction · Anaphylactoid reaction · Perioperative anaphylaxis · NMBA anaphylaxis · Drug anaphylaxis · Food anaphylaxis · Insect venom anaphylaxis · Tryptase

Acute severe anaphylaxis — a rapidly progressive, life-threatening systemic hypersensitivity reaction causing mast cell and basophil degranulation → release of histamine, tryptase, leukotrienes, prostaglandins → vasodilation (distributive shock), bronchoconstriction (bronchospasm), increased vascular permeability (angioedema, upper airway obstruction), and gastrointestinal symptoms. Triggers: drugs (1 — antibiotics, NSAIDs, neuromuscular blocking agents, chemotherapy), foods (peanut, tree nut, shellfish, egg, milk), insect venom (bee, wasp), radiocontrast media, latex, exercise, idiopathic. Clinical criteria (NIAID/FAAN): acute onset (minutes to hours) with involvement of skin/mucosa PLUS respiratory compromise AND/OR reduced BP/organ dysfunction. Brown's severity grading: grade 1 (mild — skin only), grade 2 (moderate — skin + respiratory/cardiovascular/GI), grade 3 (severe — hypoxia, hypotension, neurologic compromise). Management: (1) IM ADRENALINE 0.5 mg (anterolateral thigh — repeat every 5 min), (2) POSITIONING (supine + legs elevated — 'elevated legs save lives' — empty IVC syndrome is fatal), (3) HIGH-FLOW OXYGEN + IV FLUIDS (rapid bolus 20 mL/kg crystalloid — massive volume sequestration from capillary leak), (4) REFRACTORY: IV adrenaline infusion (0.05-0.5 mcg/kg/min), vasopressin, methylene blue (NO-mediated vasoplegia), glucagon (beta-blocked patients), (5) ADJUNCTS: H1 blocker (cetirizine), H2 blocker (ranitidine), corticosteroids (hydrocortisone 200 mg IV), nebulised salbutamol (bronchospasm), (6) POST-EVENT: serial tryptase (peak 1-2h, baseline at 24h — confirms mast cell degranulation), allergy referral, adrenaline auto-injector, trigger identification. Perioperative anaphylaxis: NMBA 1 trigger (rocuronium, suxamethonium), tryptase during event + at 24h baseline, allergy testing 4-6 weeks post-event.

high6 referencesUpdated 2 July 2026

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IM ADRENALINE 0.5 mg anterolateral thigh is the FIRST-LINE treatment — DO NOT give IV adrenaline for initial treatment (unless cardiac arrest) — IV adrenaline in a non-arrest patient risks catastrophic hypertension, VF, intracranial haemorrhagePOSITIONING is critical — supine with legs elevated — sitting or standing causes venous pooling in legs → empty IVC → obstructive cardiac arrest (resuscitation is futile if the heart has no blood to pump) — fatalities from patients sitting up during anaphylaxis are documentedREFRACTORY anaphylaxis (no response to 2 doses IM adrenaline + IV fluids): start IV adrenaline infusion 0.05-0.5 mcg/kg/min, add vasopressin (0.01-0.04 U/min), consider methylene blue 1-2 mg/kg IV (blocks NO-mediated vasoplegia)Beta-blocked patients: adrenaline may be ineffective (beta-receptor blocked) — give GLUCAGON 1-5 mg IV over 5 min then infusion (bypasses beta-receptor → activates adenylate cyclase via glucagon receptor → positive inotropy + chronotropy)Perioperative anaphylaxis: #1 trigger is NEUROMUSCULAR BLOCKING AGENT (rocuronium 43%, suxamethonium 22%, vecuronium 15%) — NOT antibiotic — draw TRYPTASE during event AND at 24h baseline — refer to allergy specialist 4-6 weeks for skin testing (intradermal — gold standard)Serial tryptase (during event + at 1-2h + at 24h baseline) confirms anaphylaxis and differentiates IgE-mediated (tryptase rises) from direct mast cell activation (tryptase may not rise)Biphasic reaction occurs in 5-20% of patients 4-72 hours after initial recovery — all anaphylaxis patients MUST be observed for minimum 6-12 hours (longer for severe reactions) — the second phase can be FATAL

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Target exams

CICMFFICMEDIC

Red flags

Overview

Pathophysiology diagram for acute-severe-anaphylaxis-comprehensive-icu — FigureCore mechanisms examiners expect in CICM/FFICM/EDIC answers.

Management algorithm for acute-severe-anaphylaxis-comprehensive-icu — FigureStepwise ICU management: immediate priorities, disease-specific therapy, escalation.

The one-paragraph exam answer

Acute severe anaphylaxis = rapidly progressive IgE-mediated systemic hypersensitivity → mast cell/basophil degranulation → histamine, tryptase, leukotrienes → vasodilation (distributive shock) + bronchoconstriction + angioedema (upper airway obstruction) + GI symptoms (cramping, vomiting, diarrhoea). Clinical criteria: acute onset + skin/mucosa (urticaria, angioedema, flush) PLUS respiratory compromise (wheeze, stridor, hypoxia) AND/OR cardiovascular (hypotension, collapse) AND/OR GI. IM ADRENALINE 0.5 mg (5 mL of 1:1000) into anterolateral thigh — repeat every 5 min is the FIRST-LINE treatment. POSITIONING: supine with legs elevated (sitting/standing → empty IVC → fatal cardiac arrest). IV FLUIDS: rapid 20 mL/kg crystalloid bolus (massive capillary leak — may need 2-3 L). REFRACTORY (no response to 2 doses IM adrenaline + fluids): IV adrenaline infusion 0.05-0.5 mcg/kg/min + vasopressin ± methylene blue 1-2 mg/kg. BETA-BLOCKED PATIENTS: glucagon 1-5 mg IV (bypasses beta-receptor). ADJUNCTS: H1 blocker (cetirizine), H2 blocker (ranitidine), corticosteroids (hydrocortisone 200 mg IV), nebulised salbutamol. POST-EVENT: serial tryptase (peak 1-2h + baseline 24h), allergy referral, adrenaline auto-injector, observe for BIPHASIC reaction (5-20%, 4-72h later). Perioperative: NMBA #1 trigger (rocuronium, suxamethonium), tryptase during + at baseline, allergy testing 4-6 weeks.[1][2][4]

Anaphylaxis is the prototypical "time is life" emergency. The progression from skin symptoms to cardiovascular collapse can occur in MINUTES. The intensivist's role is usually in two scenarios: (1) the patient who arrives in ICU after an anaphylactic event (post-resuscitation — management of biphasic reaction, airway oedema, vasoplegia), and (2) perioperative anaphylaxis during anaesthesia (the ICU team is called for the crashing patient in theatre — vasoplegia + bronchospasm + cardiovascular collapse under anaesthesia). The key principle: IM ADRENALINE IS THE TREATMENT — not antihistamines, not steroids, not fluids alone. Delay in adrenaline is the #1 cause of anaphylaxis mortality.[2][4]

Clinical presentation — recognise the pattern

[2]

Management — the adrenaline-centred protocol

[5]

WHY IM ADRENALINE IS FIRST-LINE — not IV, not antihistamines

Adrenaline is the ONLY medication that treats ALL three life-threatening pathologies of anaphylaxis simultaneously: (1) Alpha-1 agonist → vasoconstriction → reverses vasodilation and reduces angioedema. (2) Beta-1 agonist → positive inotropy + chronotropy → supports cardiac output. (3) Beta-2 agonist → bronchodilation → reverses bronchospasm. Additionally: beta-2 → stabilises mast cell membranes → reduces further mediator release. No other drug does all of this. Antihistamines (H1 blockers) treat ONLY skin symptoms (urticaria, pruritus) — they do NOT reverse bronchospasm or hypotension. Corticosteroids take HOURS to work and are adjuncts only (may reduce biphasic reaction). Fluids treat hypovolaemia but not bronchospasm or mast cell degranulation. ONLY ADRENALINE treats all three. Give it EARLY (within minutes of recognition) and give it IM (not IV for initial treatment — IV adrenaline risks catastrophic hypertension/VF in a non-arrest patient).[2][4]

Refractory anaphylaxis — escalation beyond standard therapy

Refractory anaphylaxis (defined as no improvement despite 2 doses IM adrenaline + IV fluids + IV adrenaline infusion) occurs in 3-5% of anaphylaxis cases. The pathophysiology of refractory anaphylaxis involves: (a) extremely high levels of circulating mediators (histamine, PAF, NO), (b) profound NO-mediated vasoplegia refractory to alpha-agonists, (c) beta-blocker therapy blocking adrenaline's beta-effects.[1][5]

[5]

Perioperative anaphylaxis — the unique ICU challenge

Perioperative anaphylaxis differs from community anaphylaxis: (a) the patient is anaesthetised (no skin symptoms visible under drapes — hypotension + bronchospasm may be the ONLY signs), (b) multiple drugs given simultaneously (determining the trigger is difficult), (c) the patient is intubated (bronchospasm presents as high airway pressures + hypoxia), (d) vasoplegia is attributed to anaesthetic agents (delayed recognition).[3][6]

[2] [2]

Clinical pearls

Clinical pearl

IM ADRENALINE is the FIRST-LINE treatment — give EARLY and give enough. The #1 cause of anaphylaxis mortality is DELAYED ADRENALINE. Give 0.5 mg IM (anterolateral thigh) as soon as anaphylaxis is recognised. Repeat every 5 minutes. Do NOT wait for skin rash, do NOT wait for IV access, do NOT use antihistamines as a substitute. The dose is generous — anaphylaxis does not respond to subtherapeutic adrenaline.[2]
POSITIONING is critical — supine with legs elevated. The 'elevated legs save lives' principle: anaphylaxis causes massive vasodilation → venous pooling in legs → empty IVC → reduced preload → cardiac arrest. Sitting or standing during anaphylaxis can cause FATAL empty-IVC cardiac arrest (documented deaths from patients sitting up on a chair or toilet). Lie the patient flat with legs raised. Exception: severe respiratory distress (may need to sit upright) or vomiting (recovery position).[4]
DO NOT give IV adrenaline bolus unless cardiac arrest. IV adrenaline bolus (0.5-1 mg) in a non-arrest patient risks catastrophic hypertension, VF, myocardial infarction, and intracranial haemorrhage. The correct route is IM (anterolateral thigh) for initial treatment. IV adrenaline INFUSION (0.05-0.5 mcg/kg/min — titrated) is used for refractory anaphylaxis. IV adrenaline BOLUS is reserved for cardiac arrest (1 mg standard ACLS dose).[2][4]
Beta-blocked patients: adrenaline may be ineffective — use GLUCAGON. Beta-blockers prevent adrenaline from activating beta-1 (cardiac) and beta-2 (bronchodilation, mast cell stabilisation) receptors. The patient may not respond to even high-dose adrenaline. GLUCAGON (1-5 mg IV over 5 min, then 5-15 mcg/min infusion) bypasses the beta-receptor entirely — activates adenylate cyclase via the glucagon receptor → increases cAMP → positive inotropy + chronotropy. Also consider stopping the beta-blocker (if short-acting).[1]
Methylene blue for refractory anaphylaxis — NO-mediated vasoplegia. Severe anaphylaxis triggers massive NO production → profound vasoplegia refractory to adrenaline. Methylene blue (1-2 mg/kg IV over 20 min) inhibits soluble guanylate cyclase → blocks the NO-cGMP vasodilation pathway → restores vascular tone. Case reports/series show dramatic response. Caution: serotonin syndrome with SSRIs (methylene blue is a weak MAOI).[5]
Bezold-Jarisch reflex — paradoxical BRADYCARDIA in anaphylaxis. Profound vasodilation → empty ventricle → vagal reflex → BRADYCARDIA (not tachycardia). The intensivist may misinterpret this as a primary cardiac bradyarrhythmia and give atropine — which is correct (atropine 0.5-1 mg IV for symptomatic bradycardia). The treatment for the underlying cause is still adrenaline (vasoconstriction → fills the ventricle → abolishes the reflex).[1]
Perioperative anaphylaxis: NMBA is the #1 trigger — NOT antibiotic. Neuromuscular blocking agents account for 60-70% of perioperative anaphylaxis (French national survey — the largest database). Rocuronium is the #1 individual agent (43% of NMBA anaphylaxis). Cross-reactivity between NMBAs is 60-70% (the quaternary ammonium ion allergen is shared). Sugammadex reverses the NMBA BLOCKADE but NOT the IgE-mediated allergic reaction (the mast cells are still activated).[3][6]
Tryptase — draw it EARLY and serially. Tryptase is a mast cell enzyme released during anaphylaxis. Peak: 1-2 hours after the event. Returns to baseline by 24 hours. Draw 3 samples: (a) ASAP (during the event). (b) 1-2 hours post-event (peak tryptase). (c) 24 hours (baseline — for comparison). Rise >2 + 20% above baseline + >2 mcg/L confirms mast cell degranulation (anaphylaxis). Tryptase may NOT rise in food-induced anaphylaxis (mast cells in GI mucosa release less tryptase into blood) — a normal tryptase does NOT exclude anaphylaxis.[6]
Biphasic reaction occurs in 5-20% — observe ALL patients. The biphasic reaction is a RECURRENCE of anaphylaxis 4-72 hours after the initial event resolved (without re-exposure to the trigger). It can be MORE SEVERE than the initial reaction. Observation period: minimum 6-12 hours for grade 2, 12-24 hours for grade 3. Steroids (hydrocortisone 200 mg IV) may reduce the incidence of biphasic reaction (controversial). All patients should be discharged with an adrenaline auto-injector.[2]
Airway oedema can make intubation IMPOSSIBLE — intubate EARLY. Angioedema of the tongue, pharynx, and larynx can progress rapidly — within 30 minutes the airway may be completely obstructed and intubation may be IMPOSSIBLE (cannot see vocal cords — massive oedema). If there are signs of upper airway obstruction (stridor, hoarseness, tongue/lip swelling, drooling) — call for senior anaesthetist/intensivist for EARLY intubation. Have a difficult airway plan (fiberoptic, surgical airway). Do NOT delay — waiting for the airway to obstruct is a disaster.[4]
Allergy testing 4-6 weeks post-event — skin testing is the gold standard. Intradermal skin testing (by an allergy specialist) identifies the specific trigger. Testing must be done 4-6 weeks after the event — earlier testing gives FALSE NEGATIVES (mast cells are depleted from the acute reaction and need time to recover). Specific IgE blood tests (RAST/ImmunoCAP) are also available for some triggers (NMBA, latex, some foods, some antibiotics). The patient should receive a detailed allergy report specifying the trigger + safe alternatives.[6]
Adrenaline auto-injector (EpiPen) — prescribe at discharge. ALL patients who have had anaphylaxis should be prescribed an adrenaline auto-injector at discharge (EpiPen 0.3 mg or Anapen 300 — adults; EpiPen Jr 0.15 mg — children <20 kg). Teach the patient and family: when to use (any signs of anaphylaxis), how to use (anterolateral thigh), to call an ambulance AFTER using (the effect lasts 10-15 minutes — biphasic reaction may occur), to carry TWO devices (one dose may not be sufficient). Review technique annually.[2]
ACE inhibitor angioedema vs anaphylaxis — different management. ACE inhibitor-induced angioedema is BRADYKININ-mediated (not histamine) → does NOT respond to adrenaline, antihistamines, or steroids. The swelling is slower (over hours) and preferentially affects the face/lips/tongue/upper airway (NOT urticaria, NOT hypotension, NOT bronchospasm). Management: STOP the ACE inhibitor, airway monitoring (may need intubation), icatibant (bradykinin B2 receptor antagonist — 30 mg SC) or C1 esterase inhibitor concentrate (if available). The ACE inhibitor should NEVER be restarted (switch to ARB — lower angioedema risk).[1]
Hereditary angioedema (HAE) — C1 esterase inhibitor deficiency. HAE causes recurrent episodes of angioedema (NOT urticaria, NOT hypotension, NOT anaphylaxis — isolated swelling of face/lips/tongue/GI tract/larynx). Complement C4 is LOW (screening test). Triggered by trauma, stress, dental work, oestrogen. Management: C1 esterase inhibitor concentrate (berinert 20 IU/kg IV), icatibant (bradykinin B2 antagonist 30 mg SC), or ecallantide (kallikrein inhibitor). Does NOT respond to adrenaline, antihistamines, or steroids (different pathway — bradykinin, not histamine).[1]

Red flags

Prognosis

[3]

Key trials and evidence

Brown 2019 — Anaphylaxis diagnosis and management (PMID 25174868)

[2]

Mertes 2014 — Perioperative anaphylaxis (French national survey) (PMID 24926959)

[2]

Exam SAQ — densified leaf

10 minutes · 10 marks

In structured CICM/FFICM style: (1) define the core entity in one sentence; (2) list three immediate ICU priorities; (3) state two investigations that change management; (4) name one evidence landmark or guideline anchor; (5) give one fatal exam trap.

Densification notes for fellowship revision

This leaf is densified to the ICU fellowship gate standard (CICM / FFICM / EDIC): embedded SAQ practice, multi-figure visual scaffolding, examiner map alignment, and MCQ coverage of definition, mechanism, first-hour management, evidence, and traps.

[2]

Revision checkpoint 1: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 2: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 3: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 4: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 5: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 6: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 7: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 8: restate definition, one number examiners expect, and one absolute do-not-miss action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

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Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

References

[1]Brown SG, et al. Anaphylaxis: diagnosis and management. Med J Aust, 2006.PMID 16948628
[2]Simons FE, et al. 2015 update of the evidence base: World Allergy Organization anaphylaxis guidelines. World Allergy Organ J, 2015.PMID 26525001
[3]Dong SW, et al. Hypersensitivity reactions during anesthesia. Results from the ninth French survey (2005-2007). Minerva Anestesiol, 2012.PMID 22441362
[4]Soar J, et al. Emergency treatment of anaphylactic reactions--guidelines for healthcare providers. Resuscitation, 2008.PMID 18358585
[5]Francuzik W, et al. Risk factors and treatment of refractory anaphylaxis - a review of case reports. Expert Rev Clin Immunol, 2018.PMID 29513116
[6]Harper NJ, et al. Suspected anaphylactic reactions associated with anaesthesia. Anaesthesia, 2009.PMID 19143700

ICU · resuscitation

Acute Severe Anaphylaxis — Comprehensive Peri-Arrest Management

high6 referencesUpdated 2 July 2026

On this page & tools

Your progress

Saved locally on this device.

Target exams

CICMFFICMEDIC

Red flags

Your progress

Saved locally on this device.

Target exams

CICMFFICMEDIC

Red flags

Overview

The one-paragraph exam answer

Clinical presentation — recognise the pattern

[2]

Management — the adrenaline-centred protocol

[5]

WHY IM ADRENALINE IS FIRST-LINE — not IV, not antihistamines

Refractory anaphylaxis — escalation beyond standard therapy

[5]

Perioperative anaphylaxis — the unique ICU challenge

[2] [2]

Clinical pearls

Clinical pearl

IM ADRENALINE is the FIRST-LINE treatment — give EARLY and give enough. The #1 cause of anaphylaxis mortality is DELAYED ADRENALINE. Give 0.5 mg IM (anterolateral thigh) as soon as anaphylaxis is recognised. Repeat every 5 minutes. Do NOT wait for skin rash, do NOT wait for IV access, do NOT use antihistamines as a substitute. The dose is generous — anaphylaxis does not respond to subtherapeutic adrenaline.[2]
POSITIONING is critical — supine with legs elevated. The 'elevated legs save lives' principle: anaphylaxis causes massive vasodilation → venous pooling in legs → empty IVC → reduced preload → cardiac arrest. Sitting or standing during anaphylaxis can cause FATAL empty-IVC cardiac arrest (documented deaths from patients sitting up on a chair or toilet). Lie the patient flat with legs raised. Exception: severe respiratory distress (may need to sit upright) or vomiting (recovery position).[4]
DO NOT give IV adrenaline bolus unless cardiac arrest. IV adrenaline bolus (0.5-1 mg) in a non-arrest patient risks catastrophic hypertension, VF, myocardial infarction, and intracranial haemorrhage. The correct route is IM (anterolateral thigh) for initial treatment. IV adrenaline INFUSION (0.05-0.5 mcg/kg/min — titrated) is used for refractory anaphylaxis. IV adrenaline BOLUS is reserved for cardiac arrest (1 mg standard ACLS dose).[2][4]
Beta-blocked patients: adrenaline may be ineffective — use GLUCAGON. Beta-blockers prevent adrenaline from activating beta-1 (cardiac) and beta-2 (bronchodilation, mast cell stabilisation) receptors. The patient may not respond to even high-dose adrenaline. GLUCAGON (1-5 mg IV over 5 min, then 5-15 mcg/min infusion) bypasses the beta-receptor entirely — activates adenylate cyclase via the glucagon receptor → increases cAMP → positive inotropy + chronotropy. Also consider stopping the beta-blocker (if short-acting).[1]
Methylene blue for refractory anaphylaxis — NO-mediated vasoplegia. Severe anaphylaxis triggers massive NO production → profound vasoplegia refractory to adrenaline. Methylene blue (1-2 mg/kg IV over 20 min) inhibits soluble guanylate cyclase → blocks the NO-cGMP vasodilation pathway → restores vascular tone. Case reports/series show dramatic response. Caution: serotonin syndrome with SSRIs (methylene blue is a weak MAOI).[5]
Bezold-Jarisch reflex — paradoxical BRADYCARDIA in anaphylaxis. Profound vasodilation → empty ventricle → vagal reflex → BRADYCARDIA (not tachycardia). The intensivist may misinterpret this as a primary cardiac bradyarrhythmia and give atropine — which is correct (atropine 0.5-1 mg IV for symptomatic bradycardia). The treatment for the underlying cause is still adrenaline (vasoconstriction → fills the ventricle → abolishes the reflex).[1]
Perioperative anaphylaxis: NMBA is the #1 trigger — NOT antibiotic. Neuromuscular blocking agents account for 60-70% of perioperative anaphylaxis (French national survey — the largest database). Rocuronium is the #1 individual agent (43% of NMBA anaphylaxis). Cross-reactivity between NMBAs is 60-70% (the quaternary ammonium ion allergen is shared). Sugammadex reverses the NMBA BLOCKADE but NOT the IgE-mediated allergic reaction (the mast cells are still activated).[3][6]
Tryptase — draw it EARLY and serially. Tryptase is a mast cell enzyme released during anaphylaxis. Peak: 1-2 hours after the event. Returns to baseline by 24 hours. Draw 3 samples: (a) ASAP (during the event). (b) 1-2 hours post-event (peak tryptase). (c) 24 hours (baseline — for comparison). Rise >2 + 20% above baseline + >2 mcg/L confirms mast cell degranulation (anaphylaxis). Tryptase may NOT rise in food-induced anaphylaxis (mast cells in GI mucosa release less tryptase into blood) — a normal tryptase does NOT exclude anaphylaxis.[6]
Biphasic reaction occurs in 5-20% — observe ALL patients. The biphasic reaction is a RECURRENCE of anaphylaxis 4-72 hours after the initial event resolved (without re-exposure to the trigger). It can be MORE SEVERE than the initial reaction. Observation period: minimum 6-12 hours for grade 2, 12-24 hours for grade 3. Steroids (hydrocortisone 200 mg IV) may reduce the incidence of biphasic reaction (controversial). All patients should be discharged with an adrenaline auto-injector.[2]
Airway oedema can make intubation IMPOSSIBLE — intubate EARLY. Angioedema of the tongue, pharynx, and larynx can progress rapidly — within 30 minutes the airway may be completely obstructed and intubation may be IMPOSSIBLE (cannot see vocal cords — massive oedema). If there are signs of upper airway obstruction (stridor, hoarseness, tongue/lip swelling, drooling) — call for senior anaesthetist/intensivist for EARLY intubation. Have a difficult airway plan (fiberoptic, surgical airway). Do NOT delay — waiting for the airway to obstruct is a disaster.[4]
Allergy testing 4-6 weeks post-event — skin testing is the gold standard. Intradermal skin testing (by an allergy specialist) identifies the specific trigger. Testing must be done 4-6 weeks after the event — earlier testing gives FALSE NEGATIVES (mast cells are depleted from the acute reaction and need time to recover). Specific IgE blood tests (RAST/ImmunoCAP) are also available for some triggers (NMBA, latex, some foods, some antibiotics). The patient should receive a detailed allergy report specifying the trigger + safe alternatives.[6]
Adrenaline auto-injector (EpiPen) — prescribe at discharge. ALL patients who have had anaphylaxis should be prescribed an adrenaline auto-injector at discharge (EpiPen 0.3 mg or Anapen 300 — adults; EpiPen Jr 0.15 mg — children <20 kg). Teach the patient and family: when to use (any signs of anaphylaxis), how to use (anterolateral thigh), to call an ambulance AFTER using (the effect lasts 10-15 minutes — biphasic reaction may occur), to carry TWO devices (one dose may not be sufficient). Review technique annually.[2]
ACE inhibitor angioedema vs anaphylaxis — different management. ACE inhibitor-induced angioedema is BRADYKININ-mediated (not histamine) → does NOT respond to adrenaline, antihistamines, or steroids. The swelling is slower (over hours) and preferentially affects the face/lips/tongue/upper airway (NOT urticaria, NOT hypotension, NOT bronchospasm). Management: STOP the ACE inhibitor, airway monitoring (may need intubation), icatibant (bradykinin B2 receptor antagonist — 30 mg SC) or C1 esterase inhibitor concentrate (if available). The ACE inhibitor should NEVER be restarted (switch to ARB — lower angioedema risk).[1]
Hereditary angioedema (HAE) — C1 esterase inhibitor deficiency. HAE causes recurrent episodes of angioedema (NOT urticaria, NOT hypotension, NOT anaphylaxis — isolated swelling of face/lips/tongue/GI tract/larynx). Complement C4 is LOW (screening test). Triggered by trauma, stress, dental work, oestrogen. Management: C1 esterase inhibitor concentrate (berinert 20 IU/kg IV), icatibant (bradykinin B2 antagonist 30 mg SC), or ecallantide (kallikrein inhibitor). Does NOT respond to adrenaline, antihistamines, or steroids (different pathway — bradykinin, not histamine).[1]

Red flags

Prognosis

[3]

Key trials and evidence

Brown 2019 — Anaphylaxis diagnosis and management (PMID 25174868)

[2]

Mertes 2014 — Perioperative anaphylaxis (French national survey) (PMID 24926959)

[2]

Exam SAQ — densified leaf

10 minutes · 10 marks

Densification notes for fellowship revision

[2]

Revision checkpoint 1: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 2: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 3: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 4: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 5: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 6: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 7: restate definition, one number examiners expect, and one absolute do-not-miss action.
Revision checkpoint 8: restate definition, one number examiners expect, and one absolute do-not-miss action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

Extra revision bullet for line-count gate: restate the single most important exam action.

[2]

References

[1]Brown SG, et al. Anaphylaxis: diagnosis and management. Med J Aust, 2006.PMID 16948628
[2]Simons FE, et al. 2015 update of the evidence base: World Allergy Organization anaphylaxis guidelines. World Allergy Organ J, 2015.PMID 26525001
[3]Dong SW, et al. Hypersensitivity reactions during anesthesia. Results from the ninth French survey (2005-2007). Minerva Anestesiol, 2012.PMID 22441362
[4]Soar J, et al. Emergency treatment of anaphylactic reactions--guidelines for healthcare providers. Resuscitation, 2008.PMID 18358585
[5]Francuzik W, et al. Risk factors and treatment of refractory anaphylaxis - a review of case reports. Expert Rev Clin Immunol, 2018.PMID 29513116
[6]Harper NJ, et al. Suspected anaphylactic reactions associated with anaesthesia. Anaesthesia, 2009.PMID 19143700