GC093 Urticaria, Angioedema And Anaphylaxis
Urticaria, angioedema, and anaphylaxis represent a spectrum of hypersensitivity reactions ranging from localized mast cell–mediated wheals and submucosal swelling to a severe, systemic, life-threatening allergic response involving multiorgan dysfunction.
Urticaria, Angioedema and Anaphylaxis
This lecture, delivered by Dr Philip H Li (Immunology & Allergy, HKU), is the definitive GC lecture on the clinical spectrum from wheals to anaphylaxis. The central organizing principle is that not everything that looks like an "allergy" is an allergy, and the pathomechanism (histaminergic vs bradykinergic) determines your entire clinical approach — from investigations to emergency management to long-term counselling.
Why this matters for exams: HKUMed in-house papers consistently test the ability to classify angioedema by mechanism, manage anaphylaxis acutely with the correct first-line drug, and distinguish chronic spontaneous urticaria from allergic reactions. Past papers (2024 Q40, Q94; 2023 Q92) have directly examined these concepts.
Learning Objectives (directly from slides) [1]
- Define and describe basic features of urticaria, wheals, angioedema, and anaphylaxis
- Differentiate between histamine- and bradykinin-mediated angioedema
- List common causes and investigations of urticaria
- Appreciate epidemiology and common causes of anaphylaxis in Hong Kong
- Understand pathophysiology and possible causes of bradykinin-mediated angioedema
- Describe treatment approach to chronic spontaneous urticaria
- Understand the approach to management of histaminergic urticaria and anaphylaxis
1. Core Definitions — Getting the Language Right
High Yield: Not everything is 'allergy'
The lecture opens with this critical framing. Exam questions will test whether you understand that urticaria can be non-allergic (autoimmune, spontaneous) and that angioedema can be non-histaminergic (bradykinin-mediated). The word "allergy" strictly means an immunological reaction, most commonly IgE-mediated. [1]
Three defining features of wheals: (1) Central swelling, (2) Pruritus, (3) Fleeting nature — resolves within < 24 hours [1]
Why each feature matters:
- Central swelling: Caused by localized dermal oedema from mast cell degranulation → histamine release → increased capillary permeability
- Pruritus: Histamine stimulates sensory nerve endings (C-fibres) in the superficial dermis
- Fleeting ( < 24 hours): This is the key discriminator from urticarial vasculitis. If a wheal persists > 24 hours, you are dealing with a different pathology
Urticarial vasculitis = painful (not pruritic), lasts > 24 hours, has constitutional symptoms, and leaves post-inflammatory hyperpigmentation [1]
| Feature | Urticaria (Wheals) | Urticarial Vasculitis |
|---|---|---|
| Duration of individual lesion | < 24 hours | > 24 hours |
| Sensation | Pruritic | Painful/burning |
| Residual mark | None | Post-inflammatory hyperpigmentation, ecchymosis |
| Constitutional symptoms | Absent | Present (fever, arthralgia) |
| Biopsy | Dermal oedema | Leukocytoclastic vasculitis |
| Associations | Atopy, autoimmune | SLE, hepatitis B, malignancy |
Clinical test: Mark the border of a wheal with a pen → reassess at 24 hours → if still present, think vasculitis [5].
Angioedema = swelling of the deep dermis/subcutaneous tissue. Painful rather than pruritic. Slower resolution — up to 72 hours. [1]
Why it's painful, not itchy: The swelling is deeper (deep dermis and subcutaneous tissue), where there are fewer sensory itch-fibres but more pressure-sensitive nociceptors. Compare this with wheals, which sit in the superficial dermis where histamine-sensitive C-fibres are abundant.
Critical: Angioedema must be classified as with or without wheals — this determines the endotype [1]
Anaphylaxis = serious, acute, and life-threatening systemic hypersensitivity reaction [1]
Key characteristics (from both GC lecture and the Fundamentals of Allergology lecture) [1][2]:
- Acute: rapid onset (typically minutes to hours)
- Life-threatening: can cause cardiovascular collapse and death
- Multisystem: usually involves ≥ 2 organ systems
- Especially significant: cardiac or respiratory involvement
Since 2018, "urticaria" = wheals AND/OR angioedema [1]
This is a conceptual shift. Previously, "urticaria" was thought of as just wheals. Now, the umbrella term includes:
- Wheals alone
- Angioedema alone
- Angioedema with wheals
The pattern (with or without wheals) is important to distinguish between different pathomechanisms, different clinical courses, and different management. [1]
2. Pathomechanisms (Endotypes): Histaminergic vs Bradykinergic
This is the central mechanistic framework of the entire lecture. Every clinical decision flows from determining which pathway is driving the patient's symptoms.
Mast cell mediated. Activated via FcεRIα. Release of inflammatory mediators including histamine and PAF (platelet activating factor). [1]
Downstream effects of histamine [1]:
- Sensory nerve stimulation → pruritus
- Increased vascular permeability → oedema (wheals/angioedema)
- Vasodilation → erythema, hypotension (in anaphylaxis)
- Contraction of bronchial and intestinal smooth muscle → bronchospasm, abdominal cramps/diarrhoea
Can be "allergic" or "non-allergic" [1]:
- Allergic (IgE-mediated): Allergen cross-links IgE antibodies on mast cells → triggers FcεRI → Type I hypersensitivity. This is the classic pathway in food allergy, drug allergy, venom allergy, allergic rhinitis, allergic asthma
- Non-allergic: Direct mast cell activation without IgE (e.g., opioids, radiocontrast, vancomycin "red man syndrome", physical stimuli)
Mast cell independent. Bradykinin generated through activation of the plasma contact system. A vasoactive molecule causing vasodilation, swelling, and pain. Regulated by C1-esterase inhibitor. [1]
First-principles explanation: The contact system (also called the kallikrein-kinin system) normally generates bradykinin from high-molecular-weight kininogen via kallikrein. C1-esterase inhibitor (C1-INH) normally keeps this in check by inhibiting kallikrein and Factor XIIa. When C1-INH is deficient or dysfunctional, or when its breakdown is accelerated (ACEi blocks bradykinin degradation via a different route), bradykinin accumulates → vasodilation + increased permeability in deep tissues → angioedema.
Bradykinergic angioedema is characterized by: swelling attacks (angioedema), ABSENCE of wheals and pruritus, may involve face, extremities, abdomen, and most dangerously — upper airway. [1]
Why no wheals or pruritus? Because mast cells are not involved. There is no histamine release, therefore no superficial dermal itch or wheal formation. The bradykinin acts on deeper vascular beds.
Can be drug-related (ACEi), hereditary, or acquired. [1]
| Feature | Histaminergic | Bradykinergic |
|---|---|---|
| Mediator | Histamine (+ PAF, leukotrienes) | Bradykinin |
| Cell involved | Mast cell | None (plasma contact system) |
| Wheals | Present (with or without angioedema) | Absent |
| Pruritus | Yes | No (painful) |
| Key regulator | — | C1-esterase inhibitor |
| Response to antihistamines | Yes | No |
| Response to adrenaline | Yes | Limited/variable |
| Response to steroids | Adjunctive | No |
| Specific treatment | Antihistamines, omalizumab | C1-INH concentrate, icatibant, ecallantide |
Exam Discriminator
A common exam trap: Angioedema WITHOUT wheals that does NOT respond to antihistamines → think bradykinergic. If the stem mentions ACEi use, this is almost certainly ACEi-induced angioedema. If no ACEi and family history of swelling episodes → hereditary angioedema.
3. Clinical Classification (Phenotypes)
Urticaria (wheals ± angioedema) → Always histaminergic
Angioedema WITHOUT wheals → Could be histaminergic OR bradykinergicThis is why the presence/absence of wheals is the pivotal clinical question.
Histaminergic differentials [1]:
- "Allergic" Type I hypersensitivity (foods, drugs, venom) — mostly IgE-mediated
- Spontaneous or autoimmune urticaria and angioedema (CSU) — anti-FcεRIα antibodies on mast cells
- Inducible urticaria and angioedema
- Urticarial vasculitis
- Auto-inflammatory syndromes
Bradykinergic differentials [1]:
- ACEi-induced angioedema — exclude FIRST (~0.1% of ACEi recipients)
- Hereditary angioedema (HAE) — Type I, II, III and more; 1:10,000 population; reduced level or function of C1-esterase inhibitor
- Acquired C1-esterase inhibitor deficiency — 1:100,000 population; onset > 40 years old; associated with malignancy; low C1q level
How to distinguish HAE from acquired C1-INH deficiency:
| Feature | Hereditary Angioedema | Acquired C1-INH Deficiency |
|---|---|---|
| Age of onset | Childhood/adolescence | > 40 years |
| Family history | Positive (autosomal dominant) | Negative |
| C1q level | Normal | Low (consumed by immune complexes) |
| C4 level | Low (during and between attacks) | Low |
| C1-INH level/function | Low (Type I) or dysfunctional (Type II) | Low |
| Association | Genetic | Lymphoproliferative disorders, autoimmune disease |
4. Urticaria Classification by Duration and Trigger
Acute urticaria: < 6 weeks. Chronic urticaria: ≥ 6 weeks [1]
Spontaneous: No specific trigger or eliciting factor. Inducible: Identifiable trigger(s). [1]
| Category | Examples |
|---|---|
| Acute spontaneous | Often viral infection-associated (especially in children), idiopathic |
| Acute inducible | Allergic reaction to food, drug, venom |
| Chronic spontaneous (CSU) | Autoimmune (anti-FcεRIα or anti-IgE antibodies) |
| Chronic inducible | Dermatographism, cold, cholinergic, pressure, solar, aquagenic, vibratory |
Causes of acute urticaria (from senior notes) [5]:
- Idiopathic (~50%)
- Infection e.g. URTI (~40%)
- Drugs (~10%)
- Food ( < 1%)
Causes of chronic urticaria [5]:
- Idiopathic (~50%)
- Autoimmune (antibodies against IgE or FcεRI): 40-50%
- Chronic infection (e.g. parasites): < 5%
5. Chronic Spontaneous Urticaria (CSU) — Detailed
High Yield: CSU Definition
'Chronic' = > 6 weeks. 'Spontaneous' = NOT allergy. 'Urticaria' = hives and/or angioedema. [1]
This is the most commonly tested subtype. Examiners love to present a patient with months of recurrent hives without obvious triggers and ask for the diagnosis.
CSU is a chronic auto-inflammatory skin disease. Autoantibodies against IgE or FcεRI activate basophils and mast cells → degranulation → histamine and other mediators → bind H-receptors on endothelial cells and sensory nerves. [1]
Why "spontaneous" and not "allergic"? Because there is no exogenous allergen. The immune system is attacking itself — autoantibodies directly activate the mast cell receptor. This is fundamentally different from an IgE-mediated food allergy where an external allergen is required.
Concomitant autoimmune thyroid disease in 10% [1]
This is because CSU reflects a general autoimmune tendency. Always check thyroid function and anti-thyroid antibodies in CSU patients.
Urticaria Activity Score UAS7: number of wheals + intensity of pruritus over past 7 consecutive days [1]
This validated scoring tool is used to guide treatment decisions and assess response. Each day scores wheals (0-3) and pruritus (0-3), maximum 6/day, maximum 42/week.
| UAS7 Score | Interpretation |
|---|---|
| 0 | Complete control |
| 1-6 | Well-controlled |
| 7-15 | Mild activity |
| 16-27 | Moderate activity |
| 28-42 | Severe activity |
Identify and eliminate eliciting factors (if any). Pharmacological treatment: 4 lines of treatment. [1]
Step 1 (First-line): Second-generation antihistamines
Key principles [1]:
- Second-generation only (cetirizine, loratadine, fexofenadine, bilastine — avoid sedating first-gen like chlorpheniramine for chronic use)
- Take regularly (not PRN — you need sustained H1-receptor blockade)
- Avoid different antihistamines at the same time
- Up-dosing up to fourfold (e.g., cetirizine 10mg → up to 40mg daily)
- Safety data available for use of several years continuously
Why second-generation only? First-generation antihistamines (e.g. chlorpheniramine, diphenhydramine) cross the blood-brain barrier → sedation, anticholinergic effects, impaired psychomotor function. Second-generation are peripherally selective, non-sedating, and safer for chronic daily use.
Why up to fourfold? Standard doses block ~60-70% of H1 receptors. Quadrupling the dose can achieve ~90% receptor occupancy. The EAACI guidelines specifically endorse this escalation before adding other agents.
Step 2 (Second-line): Increase antihistamine dose to fourfold (if not already done in Step 1)
Step 3 and beyond: Personalized therapy [1]
- Omalizumab (anti-IgE monoclonal antibody)
Step 4: Cyclosporine or other immunosuppressants (for refractory cases)
HK-Specific Data
HKU Urticaria Clinic data [1]: Before immunologist review, 61.1% of patients had UAS7 ≥ 16. After review, only 10.1% had UAS7 ≥ 16. This demonstrates the significant impact of specialist-led stepwise treatment optimization. Treatment breakdown: No treatment 7%, first-line 58%, second-line 25%, third-line or above 10%.
6. Anaphylaxis — In Depth
Anaphylaxis = acute, systemic, life-threatening allergic reaction [1]
The WAO/EAACI criteria (as taught in paediatrics and supported by Adrian Lui's notes) define anaphylaxis as meeting ≥ 1 of [3]:
- Acute onset with skin/mucosal involvement + respiratory compromise OR cardiovascular compromise
- ≥ 2 of the following after exposure to likely allergen: (a) skin/mucosal involvement, (b) respiratory compromise, (c) cardiovascular compromise, (d) GI symptoms
- Hypotension after exposure to known allergen
~20% of anaphylaxis cases are labelled "idiopathic" [1]
HKU study (2020): From 2018-19, > 10% of adult patients referred to QMH Immunology Clinic were for "idiopathic" anaphylaxis. After complete allergist workup, specific causes could be identified in 90%. [1]
Despite surviving anaphylaxis, less than 1/3 of patients were prescribed an adrenaline autoinjector (AAI) prior to consultation. [1]
Compared to UK patients, HK patients had more urticaria and cardiovascular manifestations. [1]
Why this matters: "Idiopathic anaphylaxis" is a diagnosis of exclusion. The lecture stresses to keep looking for triggers/explanations [1].
| IgE-mediated | Non-IgE-mediated |
|---|---|
| Foods: peanuts, tree nuts, shellfish, egg, milk | Exercise-induced |
| Drugs: β-lactams, biologics | NSAIDs (alters arachidonic acid metabolism) |
| Venom: bee, wasp, hornet | Radiocontrast agents |
| Latex | Cold/heat |
Hidden allergens vs Anaphylaxis mimics: acute urticaria/angioedema, asthmatic attacks, vasovagal syncope, panic attacks, shock and other causes of sudden collapse/respiratory distress [1]
How to differentiate vasovagal from anaphylaxis: Vasovagal → bradycardia, pallor, no urticaria/angioedema, recovery on lying down. Anaphylaxis → tachycardia, urticaria/angioedema, hypotension that persists despite lying flat.
Co-factors: exercise, NSAIDs, alcohol, menstruation, illness, stress [1]
These lower the threshold for anaphylaxis in sensitized individuals. A classic exam scenario: wheat-dependent exercise-induced anaphylaxis (WDEIA) — the patient tolerates wheat when sedentary but develops anaphylaxis when exercising after wheat ingestion [2].
| System | Manifestations |
|---|---|
| Skin (most common) | Urticaria, angioedema, erythema, flushing, pruritus |
| Respiratory | Dyspnoea, wheezing, bronchospasm, stridor, laryngeal oedema, hoarseness |
| Cardiovascular | Tachycardia, hypotension, syncope, collapse, cardiac arrest |
| GI | Nausea, vomiting, diarrhoea, abdominal pain |
| Neurological | Dizziness, confusion, loss of consciousness |
| Ocular | Conjunctival erythema, periorbital oedema |
Perioperative anaphylaxis (from Crisis Management lecture) [7]:
- Cardiovascular collapse (88%), erythema (48%), bronchospasm (40%), angioedema (24%), cutaneous rash (13%), urticaria (8%)
- Note: skin signs may be ABSENT in severe cardiovascular collapse — don't wait for a rash to diagnose anaphylaxis!
7. Anaphylaxis Management — The QMH Pathway
First-line treatment: ADRENALINE (epinephrine) [1]
| Step | Action | Details |
|---|---|---|
| 1 | IM Adrenaline | 0.5mg (1:1000) IM into mid-outer thigh. Repeat every 5-15 min if needed [1][6] |
| 2 | Position | Supine with legs elevated (unless respiratory distress → sit up) |
| 3 | Airway | Assess, intubate if needed, cricothyrotomy if angioedema prevents intubation |
| 4 | Breathing | High-flow O₂, nebulized salbutamol for bronchospasm |
| 5 | Circulation | IV access, rapid NS bolus 1-2L |
| 6 | Adjuncts | Antihistamine (e.g. chlorphenamine 10mg IV), hydrocortisone (200mg IV) |
Critical Point
Antihistamines and steroids are ADJUNCTS, not first-line treatment for anaphylaxis. ADRENALINE is the ONLY first-line treatment. [1] A common exam mistake is listing antihistamines or steroids as the primary treatment. They help with symptom relief (antihistamines) and may reduce late-phase reactions (steroids), but neither reverses the cardiovascular collapse or bronchospasm as effectively as adrenaline.
Why adrenaline works: It acts on α1 (vasoconstriction → reverses hypotension, reduces oedema), β1 (positive inotrope/chronotrope → improves cardiac output), and β2 (bronchodilation → reverses bronchospasm; inhibits mast cell degranulation → reduces further mediator release) receptors.
Paediatric dosing [3]:
- 0.15mg (BW 7.5-25kg), 0.3mg (BW ≥ 25kg)
- Via adrenaline autoinjector (AAI): Jext or EpiPen
Acute serum tryptase: within 6 hours of onset [1] Positive: either > 11.4 ng/mL OR (Baseline + 20%) + 2 ng/mL [1]
Why tryptase? Tryptase is stored in mast cell granules and released during degranulation. A rise confirms mast cell activation and supports the diagnosis of anaphylaxis. However, normal tryptase does NOT exclude anaphylaxis [4] — food-induced anaphylaxis often has normal tryptase because food allergy may involve fewer mast cells or more basophil-predominant pathways.
Baseline serum tryptase: send blood > 24 hours after the event [1]
You need both the acute and baseline tryptase to calculate the delta. An elevated baseline tryptase ( > 11.4 ng/mL) may suggest mastocytosis — an important underlying condition to consider.
Respiratory symptoms or signs: observe for at least 6-8 hours [1] Hypotension or collapse: close monitoring for 12-24 hours [1]
Why? Biphasic reactions can occur (a second wave of symptoms 4-12 hours after initial resolution, occurring in ~5-20% of cases). The lecture slide explicitly includes "observation for biphasic reaction" in the management pathway [1].
- Comprehensive and targeted allergy history
- Ensure tryptase taken
- Patient education
- Avoidance advice
- Decision for AAI
- AAI technique training
- Return demonstration (patient demonstrates back to you)
- Trigger Allergist referral (QMH Anaphylaxis Clinic)
- Strict allergen avoidance
- Antihistamines and close observation for mild reactions
- Adrenaline autoinjector and emergency medical attention for severe reactions
- Form fist around EpiPen® and pull off grey cap
- Place black end against outer mid-thigh
- Push down HARD until a click is heard/felt, hold for 10 seconds
- Remove and massage injection site for 10 seconds
8. Bradykinergic Angioedema — Detailed
~0.1% of ACEi recipients. Must be excluded FIRST. [1]
Mechanism: ACE (angiotensin-converting enzyme) also degrades bradykinin. When ACEi blocks ACE → bradykinin accumulates → angioedema. This can occur at any time during treatment (even after years of stable use).
Management: Stop ACEi immediately. Do NOT substitute with another ACEi. ARBs have a much lower risk ( < 0.1%) and can usually be used safely.
1:10,000 population. Reduced level or function of C1-esterase inhibitor. [1]
| Type | C1-INH Level | C1-INH Function | C4 Level | Mechanism |
|---|---|---|---|---|
| Type I (85%) | Low | Low | Low | Reduced production of C1-INH |
| Type II (15%) | Normal/High | Low | Low | Dysfunctional C1-INH protein |
| Type III (rare) | Normal | Normal | Normal | Factor XII mutations, estrogen-dependent |
Why C4 is low: C1-INH also inhibits activated C1 (C1r and C1s) in the classical complement pathway. Without C1-INH → unchecked C1 activation → consumption of C4. C4 is the best screening test for HAE — it is low even between attacks.
1:100,000 population. Onset > 40 years. Associated with malignancy. Low C1q level. [1]
The key distinguishing feature from HAE is the low C1q (consumed by immune complexes in underlying lymphoproliferative disease or autoimmune disease) and late onset without family history.
These do NOT respond to antihistamines, adrenaline, or steroids (because there is no histamine or mast cell involvement):
- C1-INH concentrate (plasma-derived or recombinant): replaces the missing inhibitor
- Icatibant: bradykinin B2 receptor antagonist — blocks the action of bradykinin directly
- Ecallantide: kallikrein inhibitor — prevents bradykinin generation
- Lanadelumab: anti-kallikrein monoclonal antibody (prophylaxis)
- Berotralstat: oral kallikrein inhibitor (prophylaxis)
| Investigation | When to Order | What It Tells You |
|---|---|---|
| Acute serum tryptase | Within 6 hours of suspected anaphylaxis | Confirms mast cell degranulation |
| Baseline serum tryptase | > 24 hours after event | Detects underlying mastocytosis |
| Specific IgE / skin prick test | After acute phase, in allergy clinic | Identifies specific allergen triggers |
| C4 level | Suspected HAE/acquired C1-INH def | Screening test — low even between attacks |
| C1-INH level and function | If C4 low | Distinguishes Type I vs Type II HAE |
| C1q level | If C1-INH low and onset > 40 | Low in acquired C1-INH deficiency |
| UAS7 | CSU monitoring | Disease activity score to guide treatment |
| Thyroid function + anti-thyroid Ab | CSU workup | 10% have concomitant autoimmune thyroid disease |
| CBC, ESR, CRP | Chronic urticaria | Exclude underlying infection/inflammation |
11. Key Clinical Scenarios and Exam Approach
Answer: Chronic spontaneous urticaria (CSU) [9]
- Duration > 6 weeks → chronic
- No obvious triggers → spontaneous
- Responds to antihistamines → histaminergic
- NOT hereditary angioedema (he has HIVES, and it responds to antihistamines)
- NOT acute urticaria (duration > 6 weeks)
- NOT food allergy (no trigger identified, chronic course)
Answer: Mast cells [9]
- Anaphylaxis = IgE-mediated → allergen cross-links IgE on mast cells → FcεRI activation → degranulation → histamine release
- NOT B-lymphocytes (they produce the IgE but don't degranulate)
- NOT T-lymphocytes (Type IV, delayed)
- NOT neutrophils (innate immunity, not primary in IgE-mediated reactions)
Answer: Hen's egg [10]
- 8 major food allergens: milk, egg, soy, wheat (outgrown), nuts, peanuts, fish, shellfish (persistent)
- In young children, egg and milk are the most common food allergens
- Immediate onset (15 min) → IgE-mediated
12. Integration with Related Lectures
- Immediate reactions ( < 1 hour): IgE-mediated → urticaria, angioedema, anaphylaxis
- Delayed reactions ( > 1 hour, usually 2-4 days): T-cell mediated → maculopapular rashes, SCAR (SJS/TEN, DRESS, AGEP)
- False penicillin allergy labels are a major public health issue → 1 in 50 of HK population may need de-labelling
- For acute urticaria control: non-sedating antihistamines first-line
- Up to 4 tablets (fourfold dose) before escalating
- Pre-bullous pemphigoid can mimic urticaria → always ask if individual wheals resolve within 24 hours [12]
- Perioperative anaphylaxis: cardiovascular collapse is the most common manifestation (88%), not skin signs
13. Likely Exam Questions
Q1: A 35-year-old woman on lisinopril presents with lip and tongue swelling without wheals or pruritus. She does not respond to antihistamines.
- (a) What is the most likely diagnosis? (1 mark)
- (b) What is the pathomechanism? (2 marks)
- (c) What is your immediate management? (2 marks)
Model answer:
- (a) ACEi-induced angioedema
- (b) ACEi blocks degradation of bradykinin → bradykinin accumulation → vasodilation and increased vascular permeability in deep dermis/subcutaneous tissue → angioedema. Mast cell independent. Does not respond to antihistamines.
- (c) Stop ACEi immediately. Airway assessment and monitoring. If severe, consider icatibant (bradykinin B2 receptor antagonist) or C1-INH concentrate. Do NOT re-challenge with ACEi.
Q2: List the 4 lines of treatment for chronic spontaneous urticaria. (4 marks)
Model answer:
- Second-generation antihistamine at standard dose (e.g., cetirizine 10mg daily)
- Up-dose antihistamine to fourfold (e.g., cetirizine 40mg daily)
- Add omalizumab 300mg SC monthly
- Cyclosporine or other immunosuppressant
Q3: A patient develops anaphylaxis. Describe your immediate management and the investigations you would perform. (5 marks)
Model answer:
- IM adrenaline 0.5mg (1:1000) into mid-outer thigh — repeat every 5-15 min if needed
- Position: supine with legs elevated
- High-flow oxygen
- IV access + rapid NS bolus
- Adjuncts: IV chlorphenamine + IV hydrocortisone
- Acute serum tryptase within 6 hours
- Baseline serum tryptase > 24 hours later
- Identify potential allergens (foods, drugs, venoms within 1 hour of onset)
- Observe: 6-8 hours for respiratory symptoms, 12-24 hours for hypotension/collapse
- Pre-discharge: allergy history, AAI prescription + training, allergist referral
| Trap | Why Students Get It Wrong | Correct Answer |
|---|---|---|
| "First-line for anaphylaxis" | Students choose antihistamine or steroid | IM adrenaline |
| "CSU diagnosis" with 4-month hives | Students choose "acute urticaria" or "food allergy" | CSU ( > 6 weeks, no trigger) |
| "Angioedema without wheals, on ACEi" | Students choose hereditary angioedema | ACEi-induced (exclude first) |
| "Which cell mediates anaphylaxis?" | Students choose B-cells (produce IgE) | Mast cells (degranulate) |
| "Antihistamine type for CSU" | Students choose first-generation | Second-generation only |
High Yield Summary
1. Urticaria = wheals AND/OR angioedema (2018 guideline update)
2. Two endotypes: Histaminergic (mast cell → histamine → wheals ± angioedema ± anaphylaxis) vs Bradykinergic (contact system → bradykinin → angioedema WITHOUT wheals, painful, no response to antihistamines)
3. Acute ( < 6 wk) vs Chronic (≥ 6 wk); Spontaneous vs Inducible
4. CSU: Autoantibodies against IgE/FcεRI; treat with 2nd-gen antihistamines up to 4x dose → omalizumab 300mg/month → cyclosporine; monitor with UAS7; check thyroid
5. Anaphylaxis: Acute + life-threatening + multisystem. ADRENALINE IM is FIRST LINE. Antihistamines/steroids are ADJUNCTS only. Tryptase within 6h (acute) and > 24h (baseline). Observe 6-8h (respiratory) or 12-24h (cardiovascular). Pre-discharge: AAI training + allergist referral
6. Bradykinergic angioedema: Exclude ACEi first → then HAE (low C4, low/dysfunctional C1-INH) → then acquired (low C1q, onset > 40, malignancy). Treat with C1-INH concentrate/icatibant, NOT antihistamines
7. HK data: 90% of "idiopathic" anaphylaxis has identifiable cause after specialist workup; < 1/3 prescribed AAI before allergist review
Active Recall - Urticaria, Angioedema and Anaphylaxis
[1] Lecture slides: GC 093. Urticaria, angioedema and anaphylaxis.pdf (all pages) [2] Lecture slides: Immunology- Fundamentals of allergology.pdf; Block A - Fundamentals of Allergology.pdf [3] Senior notes: Adrian Lui Pediatrics Notes.pdf (p401-405) [4] Senior notes: Maksim Medicine Notes.pdf (p74) [5] Senior notes: Ryan Ho Rheumatology.pdf (p145) [6] Senior notes: Ryan Ho Critical Care.pdf (p24) [7] Lecture slides: Crisis Management.pdf (p10) [8] Lecture slides: GC 139. A child with atopic eczema and food allergy.pdf (p48) [9] Past papers: 2024 Fourth Summative MCQ.pdf (Q40, Q94) [10] Past papers: 2023 Fourth Summative MCQ.pdf (Q92) [11] Senior notes: Block A - Treatments for skin diseases (eczema, psoriasis and urticaria).pdf (p46) [12] Senior notes: Block A - It is red and painful (bacterial and viral skin infections).pdf (p24)
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