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Basics

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BASICS

Definition!!navigator!!

Urticaria and AG are common inflammatory reaction patterns resulting from mast cell and, to a lesser extent, basophil degranulation. AG is a focal or diffuse excessive accumulation of tissue fluid within the interstitium, often at gravitative surfaces, that presents as edematous swellings, which may exhibit serum leakage through the skin or hemorrhage. Urticarial reactions vary in severity from inconsequential to problems of a life-threatening nature.

Pathophysiology!!navigator!!

The release of cellular inflammatory mediators such as histamine, platelet-activating factor, and prostaglandins contributes to increased vascular smooth muscle relaxation and endothelial cell retraction, causing plasma to extravasate and cause turgid edematous wheals. Urticaria is classified as immunologic, immediate immunoglobulin E-mediated (type I), immune complex-mediated (type III), or delayed cell-mediated (type IV) hypersensitivities, or nonimmunologic.

Systems Affected!!navigator!!

  • Skin/exocrine
  • Respiratory

Genetics!!navigator!!

Genetic predisposition is suspected.

Incidence/Prevalence!!navigator!!

Urticaria is within the top 10 most common equine dermatoses.

Geographic Distribution!!navigator!!

Worldwide

Signalment!!navigator!!

Suspected Breed Predilections

Arabians, Thoroughbreds, Quarter Horses, and Warmbloods may be predisposed because of their propensity to develop allergic dermatitis. Larger cohorts must be compared with general hospital populations to confirm breed predispositions.

Mean Age and Range

Mean age of onset is unknown.

Predominant Sex

Equal distribution exists between males and females.

Signs!!navigator!!

General Comments

  • Onset of lesions can be acute or peracute episodes occurring 15 min to hours post challenge. Chronic urticaria is a relapsing presentation that persists for at least 6–8 weeks. The characteristic lesion is a wheal—a flat-topped papule/nodule with steep-walled sides resulting from localized transient edema within the dermis. Pitting edema is a key clinical feature of urticaria or AG, although gyrate urticaria often does not pit. Clinical classification of urticaria relies on size and appearance
  • Conventional—wheal size varies from 2–3 mm to 3–5 cm in diameter
  • Papular—wheal size is uniform and small, 3–6 mm in diameter
  • Gyrate (polycyclic)—wheals have unusual shapes such as annular, doughnut, serpiginous, aciform and can persist for months
  • Giant—single or multiple wheals that range from 20 to 40 cm in diameter
  • Exudative—severe dermal edema oozes from the skin, mats the hair, and causes alopecia, often mistaken for pyoderma, dermatophytosis, and pemphigus foliaceus
  • Linear—firm, multiple, parallel contiguous banding patterns that can be present on the sides of trunk, shoulders, forearms, flanks, gaskins, and the cranial aspects of hocks. Often permanent and nonresponsive to steroid and antihistamine therapy. Multiple horses on farm may be affected
  • AG (angioneurotic edema)—diffuse SC edema, affecting head, thorax, ventral abdomen, and/or gravity-dependent extremities

Causes!!navigator!!

Causes are either immunologic or nonimmunologic, with the former the most common.

  • Immunologic causes include:
    • Insect hypersensitivity (stinging and biting insects), atopy (pollens, molds, and epidermals), food allergy
    • Drugs (including vaccines, anthelmintics)
    • Various others such as penicillin, tetracycline, sulfonamides, neomycin, ciprofloxacin, phenylbutazone, flunixin, phenothiazines, guaifenesin, ivermectin, moxidectin, iron, dextrans, hormones, and vitamin B complex
    • Infections—bacterial (e.g. strangles, salmonellosis, botulinum,), pyoderma, cellulitis, lymphangitis, abscess, dermatophytosis, parasitic protozoal (e.g. Trypanosoma equiperdum)
    • Vasculitis (immune-mediated or photo-activated)
    • Contact with substance (e.g. leather soaps, conditioners, or rubber tack)
    • Snakebite
    • Plants (e.g. nettle and buttercup)
    • Mast cell or lymphoreticular neoplasia
    • Autogenous sweat
  • Nonimmunologic factors include psychologic stresses, genetic abnormalities, temperature (heat, cold, or sunlight), physical (pressure or dermatographism), exercise, cholinergic, and administration of radiocontrast media and opiates
  • Idiopathic—the likelihood of documenting a specific etiology of chronic urticaria is low, thus the diagnosis of “idiopathic” is common

Risk Factors!!navigator!!

  • Temperate environments with long allergy seasons
  • Concurrent pruritic dermatoses, such as insect hypersensitivity (summation effect)
  • Treatment by polypharmacy

Diagnosis

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DIAGNOSIS

Differential Diagnosis!!navigator!!

Differential diagnoses for urticaria vary with the morphologic presentation.

  • Conventional—vasculitis
  • Papular—infectious and sterile folliculitis, frequently associated with biting insects, in particular mosquitoes and Culicoides spp.
  • Giant—vasculitis
  • Gyrate—erythema multiforme, drug reactions

CBC/Biochemistry/Urinalysis!!navigator!!

  • Leukocytosis suggests inflammatory or infectious disease
  • Thrombocytopenia may be secondary to vasculitis.

Other Laboratory Tests!!navigator!!

Relevance equated to etiology.

Diagnostic Procedures!!navigator!!

  • Biopsy—used to differentiate urticaria, pyoderma, pemphigus, dermatophytosis, or vasculitis
  • Dermatographism test—scratch the skin with blunt object and observe for reaction within 10–15 min. A positive reaction is an edematous wheal that follows the path of the scratch
  • Heat- or cold-induced urticaria is confirmed by applying a reusable hand warmer or ice cube to the skin for a few minutes with the formation of a wheal within 15 min
  • Exercise-induced urticaria requires a period of active exercise to occur, whereas cholinergic urticaria results from an active (exercise) or a passive (hot bath) increase in core body temperature
  • Sweat-induced urticaria can be induced at work or with α2-adrenoreceptor agonist drugs such as detomidine hydrochloride or xylazine. An IDT with purified sweat dilutions can be used to confirm diagnosis
  • An IDT is used to identify causative allergens (pollens, molds, epidermals) for inclusion into allergen-specific immunotherapy
  • Horses with a suspected adverse reaction to food should undergo a food exclusion trial. Start with a 4–8 week trial of a novel food source such as single-source hay (alfalfa, orchard, timothy, or coastal Bermuda grass). Single-source grains include rolled oats, beet pulp, or barley. Commence food trial by eliminating all grains, supplements, and drugs, and feed single-source hay. After resolution of urticaria, confirm food allergy by rechallenging with the introduction of 1 item each week
  • A patch test is used to identify contact reactions. Clip a small area on the lateral aspect of the neck with a no. 40 blade. Place a small amount of the test substance on a piece of gauze and affix it so that the substance is in contact with the clipped area. Remove the gauze and observe for urticaria 24–48 h after application
  • Skin scrapings, fungal and bacterial cultures, and impression smears should be performed if infectious causes are suspected

Treatment

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TREATMENT

Aims!!navigator!!

Identify and eliminate the primary cause.

Appropriate Health Care!!navigator!!

Depends on etiology.

Nursing Care!!navigator!!

Frequent bathing using cool water (antimicrobial shampoos, chlorhexidine, sulfur/salicylic acid, ± colloidal oatmeal rinses, antimicrobial sprays with 1% hydrocortisone or leave-on conditioners) removes allergens, crusts, bacteria, and debris, controls secondary infections, hydrates skin, and counters pruritus.

Activity!!navigator!!

Determined by severity and cause.

Diet!!navigator!!

Essential fatty acid supplementation may be beneficial. Omega 3 fatty acids provide EPA and DHA for anti-inflammatory and skin barrier support.

Client Education!!navigator!!

Depends on etiology.

Medications

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MEDICATIONS

Drug(s) of Choice!!navigator!!

  • Glucocorticoids are indicated to break the cycle of mediator-induced inflammation. Use a rapid-acting glucocorticoid such as prednisolone sodium succinate (0.25–10.0 mg/kg IV)
  • If refractory to antihistamine therapy, use oral prednisolone at 0.5–1.5 mg/kg every 24 h until control achieved; then reduce to lowest dose alternate-day regimen, e.g. 0.2–0.5 mg/kg every 48 h
  • If refractory to prednisolone, try dexamethasone at initial loading oral or IV dose of 0.02–0.1 mg/kg PO every 24 h for 2–4 days followed by oral maintenance dose of 0.01–0.02 mg/kg every 48–72 h for maintenance
  • Repository injectable corticosteroids should be avoided as withdrawal upon an adverse reaction is not possible
  • Antihistamines—hydroxyzine hydrochloride or pamoate at 1–2 mg/kg PO every 8–12 h or cetirizine hydrochloride at 0.4 mg/kg PO every 12 h or chlorpheniramine (chlorphenamine) at 0.25–0.5 mg/kg PO every 12 h may be effective

Contraindications!!navigator!!

  • Because of the anticholinergic properties of antihistamines and tricyclic antidepressants, do not use in patients with a history of cardiac arrhythmias, colic, glaucoma, or urinary retention disorders. Antihistamines may thicken mucus in the respiratory tract. Use extra caution in horses with respiratory problems owing to excess mucus
  • Administration of ivermectin with cetirizine can prolong cetirizine elimination half-life through P-glycoprotein inhibition

Precautions!!navigator!!

  • Epinephrine may cause excitement in horses; if administered SC, its potent vasoconstriction activity leads to poor absorption and local tissue necrosis
  • Adverse effects of epinephrine therapy are tachyarrhythmia and myocardial ischemia
  • The use of epinephrine should be avoided with the use of α2-adrenoreceptor agonists such as xylazine or detomidine HCl as they potentate α2-agonist effects
  • Taper patients on long-term steroid therapy so endogenous steroid production resumes
  • Transient sedation may occur with antihistamines

Possible Interactions!!navigator!!

Antihistamines have an additive effect with other CNS-depressant drugs.

Follow-up

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FOLLOW-UP

Patient Monitoring!!navigator!!

Horses with respiratory and/or GI involvement should be monitored at a facility with an intensive care unit.

Prevention/Avoidance!!navigator!!

Depends on the etiology.

Possible Complications!!navigator!!

  • Most serious complication of AG is respiratory compromise
  • AG may involve the GI tract, leading to intestinal wall edema and clinical signs of colic and/or diarrhea
  • CNS signs may occur secondary to focal cerebral edema

Expected Course and Prognosis!!navigator!!

  • Prognosis is generally good to excellent for control of urticaria
  • Linear urticaria may be more difficult to control or resolve
  • Spontaneous remission occurs

Miscellaneous

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MISCELLANEOUS

Associated Conditions!!navigator!!

AG—pleural or peritoneal effusion.

Age-Related Factors!!navigator!!

Severity may worsen with age.

Pregnancy/Fertility/Breeding!!navigator!!

Antihistamines—no information on teratogenicity is available for horses.

Synonyms!!navigator!!

Hives

Abbreviations!!navigator!!

  • AG = angioedema
  • CNS = central nervous system
  • DHA = docosahexaenoic acid
  • EPA = eicosapentaenoic acid
  • GI = gastrointestinal
  • IDT = intradermal test

Suggested Reading

Fadok VA. Equine urticaria. In: Noli E, Foster A, Rosenkrantz W, eds. Veterinary Allergy. Chichester, UK: Wiley Blackwell, 2014:338343.

Author(s)

Author: Gwendolen Lorch

Consulting Editor: Gwendolen Lorch

Additional Further Reading

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