Urticaria and angioedema !
Hives are itchy raised welts that come and go within a day; angioedema is deeper swelling of the lips, eyes or tongue that can block the airway.
Updated 2026-11-01
Structures involved
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In the clinical exam
Why it happens
- Mediators of inflammation: the table to know
- Vascular changes in acute inflammation: vasodilation, leakage, exudate vs transudate
- Histamine, serotonin, bradykinin and the plasma protein cascades
- Starling forces at the capillary
- Angiotensin-converting enzyme (ACE)
- Connective tissue proper: cells and fibres
What it is
Urticaria is a transient eruption of itchy wheals caused by swelling of the superficial dermis. Angioedema is swelling of the deep dermis, subcutaneous tissue or mucosa; it may occur with hives (mast-cell type) or alone (bradykinin type, as with ACE inhibitors or hereditary angioedema).
Who gets it
Very common: about one in five people has urticaria at some time in life. Acute urticaria predominates in children; chronic spontaneous urticaria is more frequent in middle-aged women. ACE inhibitors, widely used for hypertension in Colombia, are a leading cause of isolated angioedema in emergency departments.
Causes
- Acute urticaria: infections (especially viral), foods, drugs (beta-lactams, NSAIDs) and insect stings
- Chronic spontaneous urticaria: often autoimmune (IgG against IgE or its receptor); frequently no trigger found
- Inducible urticaria: cold, pressure, heat, sun, exercise or scratching (dermographism)
- Bradykinin-mediated angioedema: ACE inhibitors, hereditary C1-inhibitor deficiency or dysfunction, acquired C1-inhibitor deficiency
Risk factors
- Atopy and other allergic disease
- Autoimmune thyroid disease (associated with chronic urticaria)
- Use of ACE inhibitors (risk higher in people of African ancestry and in smokers)
- Family history of recurrent swelling without hives (hereditary angioedema)
- NSAID use, which can worsen chronic urticaria
Pathophysiology
In urticaria, mast cells degranulate (via IgE, autoantibodies or direct stimuli) and release histamine and other mediators; vessels dilate and leak, producing wheals and flare in the superficial dermis that resolve within 24 hours. Mast-cell angioedema is the same process deeper down. Bradykinin angioedema follows excess bradykinin, from blocked breakdown (ACE inhibitors) or unchecked production (low C1 inhibitor); it does not itch, lasts 2–5 days and does not respond to antihistamines.
Classification
- Acute urticaria: under 6 weeks
- Chronic urticaria: 6 weeks or more, spontaneous or inducible
- Mast-cell (histaminergic) angioedema, usually with hives
- Bradykinin-mediated angioedema: ACE inhibitor-induced, hereditary (types I–III), acquired
Symptoms and signs
- Itchy, raised, pale-centred red wheals that change shape and fade within 24 hours without a mark
- New wheals appearing in other places
- Non-pitting swelling of the lips, eyelids, tongue, face, hands or genitals
- Burning or tight feeling in the swollen area rather than itch in bradykinin angioedema
- Colicky abdominal pain and vomiting from bowel-wall oedema in hereditary angioedema
Diagnosis
- Clinical
- Mainly clinical: the history (duration of each lesion, triggers, drugs including ACE inhibitors and NSAIDs, family history) and the appearance of wheals or swelling. The airway is checked first in any facial or oral swelling.
- Tests
- Acute urticaria usually needs no tests. Chronic urticaria: limited tests such as blood count, CRP or ESR and, depending on context, thyroid antibodies. Isolated recurrent angioedema: C4 (low in hereditary angioedema), C1-inhibitor level and function; C1q helps identify the acquired form. Serum tryptase if anaphylaxis is suspected.
- Imaging
- Not routinely needed; laryngoscopy (nasoendoscopy) assesses laryngeal oedema, and abdominal ultrasound or CT may show bowel-wall oedema during abdominal attacks.
Differential diagnosis
- Anaphylaxis (hives plus respiratory or circulatory compromise)
- Urticarial vasculitis
- Contact dermatitis or cellulitis causing facial swelling
- Insect bites and papular urticaria
- Superior vena cava syndrome or hypothyroid myxoedema as causes of facial swelling
Goal of treatment
Secure the airway when needed, remove the trigger, relieve itch and swelling, and choose treatment according to mechanism, because bradykinin angioedema does not respond to antihistamines, corticosteroids or epinephrine as mast-cell disease does.
Treatment
- Acute
- Airway first: assess for stridor and voice change, give intramuscular epinephrine if anaphylaxis is present, and prepare for advanced airway management in severe tongue or laryngeal swelling.
- Medical
- Second-generation (non-sedating) H1 antihistamines are first-line for urticaria; the dose can be increased in chronic cases, and anti-IgE therapy (omalizumab) or ciclosporin is added for refractory chronic urticaria. A short course of oral corticosteroids may be used for severe acute flares.
- Medical
- ACE inhibitor angioedema: stop the drug permanently and never restart it; switching to another class is chosen with care. Observation, since swelling can progress for hours.
- Medical
- Hereditary angioedema: attacks are treated with C1-inhibitor concentrate, a bradykinin B2 receptor antagonist (icatibant) or a kallikrein inhibitor; long-term prophylaxis in frequent attacks; fresh frozen plasma if nothing else is available.
- Lifestyle
- Avoiding identified triggers (foods, NSAIDs, physical stimuli), carrying an allergy record and, when anaphylaxis risk exists, an epinephrine autoinjector.
Complications
- Upper airway obstruction and asphyxia from laryngeal oedema
- Anaphylaxis
- Poor sleep, anxiety and reduced quality of life in chronic urticaria
- Unnecessary abdominal surgery when hereditary angioedema attacks are mistaken for an acute abdomen
Prognosis
Acute urticaria usually settles within days to weeks. Chronic spontaneous urticaria remits in about half of people within a few years. ACE inhibitor angioedema can first appear years after starting the drug and recurs if the drug is continued. Hereditary angioedema is lifelong but well controlled with modern therapy.
Prevention
- Avoiding known triggers and documenting drug reactions
- Asking about previous angioedema before starting an ACE inhibitor
- Family screening (C4, C1 inhibitor) when hereditary angioedema is diagnosed
Test yourself
Think of the answer, then tap the question to see it.
What time cut-off separates acute from chronic urticaria?
Six weeks: acute urticaria lasts less than 6 weeks and chronic urticaria 6 weeks or more.
Which mediator causes ACE inhibitor-induced angioedema?
Bradykinin, because ACE normally breaks it down; antihistamines do not work and the drug must be stopped for good.
Which screening test is low in hereditary angioedema?
Serum C4, followed by C1-inhibitor level and function.
What is the first-line drug class for chronic urticaria?
Second-generation (non-sedating) H1 antihistamines, up-dosed if needed.
What is the nursing priority in a patient with tongue swelling?
Airway: watch for stridor, hoarseness, drooling and breathing difficulty, and prepare for emergency airway management.
Related conditions
- Anaphylaxis
- Arterial hypertension
- Allergic rhinitis
- Asthma
- Hypothyroidism
- Contact dermatitis (irritant and allergic)
- Stevens–Johnson syndrome and toxic epidermal necrolysis
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Hives (MedlinePlus (U.S. National Library of Medicine), 2024); Angioedema (MedlinePlus (U.S. National Library of Medicine), 2024).
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