Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Separate mast-cell-mediated angioedema from bradykinin-mediated and other swelling, secure the airway early, and investigate recurrent episodes without misusing allergy tests.
Take a minute-by-minute history: site first affected, speed, itch, wheals, flushing, breathing, hypotension, abdominal pain, duration and response to treatment. Review ACE inhibitors, oestrogen exposure, NSAIDs and recent new drugs. Ask about dental procedures, trauma, family episodes and unexplained abdominal admissions.
The phenotype determines investigation. A single episode with classic urticaria may need no complement testing. Recurrent non-urticarial swelling warrants C4 and C1-inhibitor level and function; low C1q may support acquired disease in appropriate specialist assessment. Tryptase is relevant after suspected anaphylaxis, not as a general angioedema screen.
Clinical decisions in Angioedema with and without urticaria depend on trajectory and consequence. Re-examine evolving skin, repeat focused systemic assessment when the patient changes, and reconcile every result with morphology and timing; a normal early test cannot neutralise worsening pain, mucosal injury or organ dysfunction.
Allergens, spontaneous urticaria and some medicines release histamine and related mediators, usually causing rapid itchy swelling with wheals or other anaphylaxis features.
ACE inhibition, hereditary C1-inhibitor deficiency and acquired complement disorders increase bradykinin, producing slower non-itchy swelling without ordinary wheals.
Dental infection, cellulitis, venous obstruction, contact dermatitis, thyroid disease and dependent oedema can resemble angioedema but follow different anatomical and temporal patterns.
Mediator-driven leakage in deep dermis, subcutis and submucosa creates poorly demarcated swelling that feels tight or painful rather than forming a superficial wheal.
Mast-cell disease often evolves over minutes, accompanies itch and urticaria, and improves with H1 blockade; anaphylaxis requires adrenaline because multiple organs are threatened.
Excess bradykinin increases vascular permeability over hours, commonly affects bowel and airway, lacks wheals and responds poorly to antihistamines, corticosteroids and adrenaline.
C1-inhibitor deficiency or dysfunction permits uncontrolled contact-system activation; C4 often falls during attacks but diagnostic confirmation needs antigenic and functional assays.
Tongue, floor-of-mouth or laryngeal swelling, altered voice, drooling or stridor requires immediate airway expertise and repeated examination.
Rapid itchy lip or eyelid swelling with wheals, flushing or allergen exposure favours mast-cell activation and may be part of anaphylaxis.
Slower non-pruritic swelling without wheals, poor antihistamine response and recurrent abdominal pain suggests ACE-inhibitor or C1-inhibitor-mediated disease.
Severe episodic cramping, vomiting and ascites-like fluid shift can be bowel-wall angioedema, particularly with a matching family or swelling history.
Angioedema with acute airway, breathing or circulatory compromise is treated as anaphylaxis regardless of whether a trigger or wheal is identified.
Recurrent non-urticarial swelling, severe abdominal attacks, family history or onset when young supports C1-inhibitor deficiency, although de novo variants occur.
New non-itchy facial, oral or tongue swelling can begin after years of uneventful ACE-inhibitor treatment and mandates permanent withdrawal.
Unilateral painful erythema, fever, dental symptoms, neck mass or persistent dependent swelling suggests infection or impaired venous or lymphatic drainage.
Unilateral warmth, dental pain, fever, purulence or a persistent focal mass is not typical angioedema and needs urgent alternative assessment.
Progressive tongue and laryngeal oedema can make ventilation and intubation difficult, so early expert airway involvement is safer than waiting for stridor.
Treating bradykinin episodes repeatedly with antihistamines or corticosteroids delays effective specialist rescue therapy and adds avoidable adverse effects.
Bowel-wall oedema causes severe colicky pain, vomiting and fluid shift and can lead to unnecessary surgery before hereditary disease is recognised.
Unrecognised hereditary angioedema leaves relatives without testing, trigger counselling, procedural prophylaxis or access to effective on-demand treatment.
Ordinary urticaria strongly favours mast-cell mediation, whereas bradykinin angioedema characteristically occurs without wheals.
Years of previous tolerance do not make an ACE inhibitor innocent when new tongue or facial swelling appears.
Some hereditary attacks cause severe bowel symptoms without visible peripheral swelling and mimic an acute surgical abdomen.
A patient can have dangerous supraglottic swelling while saturation remains normal, making voice and anatomy crucial.
Failure of antihistamine and corticosteroid treatment supports but does not by itself prove a bradykinin mechanism.
Waiting for stridor or desaturation before requesting expert airway support.
Continuing an ACE inhibitor because the first angioedema episode occurred years after it was started.
Calling non-urticarial recurrent swelling an allergy and ordering indiscriminate food panels.
Using a normal single C4 result to dismiss a convincing hereditary angioedema history.
Assuming adrenaline treats the bradykinin mechanism while overlooking the need for airway care and disease-specific rescue.
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A 24-year-old has recurrent non-itchy hand swelling and severe self-limiting abdominal pain. There are no wheals, and an aunt has similar episodes. Which investigation set is most appropriate?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Use the intramuscular route initially, monitor continuously, avoid inadvertent intravenous bolus, and seek expert support for refractory anaphylaxis or a threatened difficult airway.
Somnolence, alcohol, driving, renal function, pregnancy and breastfeeding need review; a non-response should trigger mediator reassessment rather than automatic repeated dosing.