Urticaria, angio-oedema and anaphylaxis

26 Urticaria, angio-oedema and anaphylaxis


Urticaria, angio-oedema and anaphylaxis may occur as a result of a variety of different stimuli, predominantly immunological but also nonimmunological, that induce mast cell (and basophil) degranulation. The predominant immunological mechanism is a type I hypersensitivity (HS) reaction whereby antigen activates mast cells (and basophils) by binding to immunoglobulin E (IgE) molecules on surface receptors. Previous exposure to the antigen in question (sensitization) results in an exaggerated immune response and excessive production of IgE which is then available for binding to mast cells and mediating an abnormally intense response to repeat antigen exposure.


Type I HS is ‘immediate’ as a reaction occurs within seconds or minutes of antigen exposure. This may then be followed by an additional late phase reaction 6–12 hours later due to the release of mediators from activated eosinophils (and neutrophils). Nonimmunological mast cell activation does not require prior sensitization and occurs either directly or more commonly through complement activation.


Clinical signs result from the sudden and excessive release of inflammatory mediators from mast cells (and perhaps basophils) and subsequently eosinophils. The severity and location of the response depend on the number and location of the cells involved that in turn depend on the degree of sensitization of the animal (immunological), the amount of antigen involved and the route of exposure. Mast cell degranulation and mediator release can be localized or systemic in more severe cases.



Localized Reactions


Localized reactions are most common, with the site dependent on the route of antigen exposure. For example:


• Antigens affecting the skin cause localized dermatitis, urticaria (hives) and angioedema

• Inhaled/aerosolized antigens cause respiratory tract responses; may also contact the eyes causing conjunctivitis and lacrimation

• Ingested antigens cause diarrhoea (possibly haemorrhagic), abdominal pain.


Urticaria and Angio-oedema


Urticaria refers to local superficial (dermis) lesions grossly visible as discrete erythematous wheals. Lesions usually develop within 30 minutes to a few hours and are variably pruritic. Lesions usually disappear within 24–48 hours (but may be more chronic). Differential diagnoses for urticaria include:


• Superficial folliculitis

• (Early) erythema multiforme

• Vasculitis

• Neoplasia.

In angio-oedema, subcutaneous tissues and deep blood vessels become affected by the inflammatory process, resulting in oedema and consequent diffuse swelling that is usually not pruritic. Angio-oedema typically affects the face (especially around the eyes, mouth and ears) although other areas, in particular the extremities, may be involved (Figure 26.1).


image image image

Figure 26.1 (a–c) Photographs of a Boxer dog showing cutaneous erythema, urticaria and angioedema especially affecting the head.


(Photographs courtesy of Filippo de Bellis)


Angio-oedema of the laryngeal or pharyngeal mucosa may cause potentially severe upper respiratory tract obstruction. Differential diagnoses for angio-oedema include:


• Early juvenile cellulitis

• Early bacterial cellulitis

• Vasculitis

• Neoplasia.

Treatment of urticaria and angioedema is described in the case example.



Systemic Reactions – Anaphylaxis/Anaphylactic Shock


A severe sudden systemic release of inflammatory mediators from activated mast cells (and perhaps basophils) is the underlying pathogenesis of acute anaphylaxis/anaphylactic shock. The rate of mediator release exceeds the animal’s ability to compensate for their effects. The majority of mast cell mediators have vasoactive properties and systemic vascular effects are therefore most prominent.


Maldistributive shock occurs and in addition a marked increase in capillary permeability causes significant loss of fluid from the intravascular to the extravascular compartment, resulting in hypovolaemic shock (see Ch. 2). The cardiovascular picture during anaphylaxis (hypoperfusion that is refractory to appropriate fluid therapy) is also a hallmark of maldistributive shock secondary to systemic inflammatory response syndrome (SIRS) or sepsis (SIRS due to infection, most commonly bacterial). Thorough evaluation to exclude sepsis may be indicated in some cases prior to making a presumptive diagnosis of anaphylaxis.



Treatment of anaphylaxis


The aims of therapy in anaphylaxis are to correct systemic hypoperfusion and to attempt to address some of the underlying pathogenic mechanisms. If appropriate, suspected inciting causes must be discontinued and reexposure prevented. Aggressive individually tailored intravenous fluid therapy and adrenaline (epinephrine) are the mainstay of treatment, and regular monitoring of cardiovascular and other major systems is vital. Recommended doses of adrenaline (epinephrine) are:


• 0.01 mg/kg slow i.v. (or i.m., s.c. in less severe cases)

Related posts:

  1. Jaundice
  2. Shock and dehydration
  3. Pallor and approach to anaemia
  4. Oxygen supplementation

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Sep 3, 2016 | Posted by in SMALL ANIMAL | Comments Off on Urticaria, angio-oedema and anaphylaxis

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