Pruritus is defined as an unpleasant sensation within the skin that provokes the desire to scratch.

Pathophysiology

Pruritus may be well or poorly localized. It may manifest as a sharp or diffuse, burning sensation. Although the skin is richly innervated, there are no known specialized pruritus receptors. The sensation of itch is transmitted via a specialized set of afferent fibers. Myelinated fibers that conduct sensations at 10–20 m/sec carry the well-localized pricking itch sensation. In contrast, the sensation of burning itch is transmitted via nonmyelinated fibers that conduct sensations at 2 m/sec. Both of these fibers enter the dorsal root of the spinal cord, ascend through the dorsal column, and cross into the lateral spinothalamic tract. From there they go to the thalamus and on to the sensory cortex.

The mediators of pruritus are controversial and may vary depending on the species. These putative mediators include histamines (released from mast cell degranulation), proteolytic enzymes (proteases), and leukotrienes. Proteases are released by fungi, bacteria, and mast cell degranulation, and during antigen-antibody reactions. Leukotrienes, prostaglandins, and thromboxane A₂, which are broken down from arachidonic acid, are pro-inflammatory. Essential fatty acids, particularly glinolenic acid, have been used to counter the inflammation mediated by leukotrienes and thromboxane A₂. The sensation of pruritus may be affected by a variety of factors including boredom, competing sensations, and anxiety. Stress may potentiate pruritus via the release of opioid peptides.

Etiology

Pruritus is a clinical sign and not a diagnosis or specific disease. In general, the most common causes of pruritus are parasites, infections, allergic skin diseases, and miscellaneous causes (eg, cutaneous neoplasia). Many diseases that are nonpruritic (eg, endocrinopathies) become pruritic when the patient develops secondary bacterial or yeast infections.

Diagnosis

A thorough dermatologic history and physical examination should be performed. Parasitic causes of pruritus, including Demodex, fleas and ticks, contagious mites, and lice, should be ruled out, as they are most common. Skin scrapings can rule in or out various mite infestations including Demodex. However, some mite infestations (eg, Sarcoptes, Cheyletiella, Psoroptes, Chorioptes) might be missed on skin scrapings. If a mite infestation is suspected, a response to therapy trial should be undertaken. The most commonly used drug in these cases is ivermectin. Fleas can be ruled in or out on the basis of a history of flea control, response to flea control, or finding evidence of flea infestation via a flea combing. Flea control practices will also rule out louse infestations.

The next most important group of pruritic diseases to rule out is infectious causes of skin disease. These include bacterial infections (primarily staphylococcal infections, Malassezia overgrowth, and dermatophytosis). A fungal culture should be performed in any cat presented for pruritus. It is also highly recommended in dogs that are newly acquired, any animal with a possible history of exposure and/or compatible clinical signs, or when there is a history of humans with skin disease. Concurrent bacterial and yeast infections are increasingly recognized as a common cause of pruritus in dogs, cats, and large animals. Bacterial pyoderma is underdiagnosed in cats, and a response to therapy trial may be needed to rule it in or out.

Infectious causes of pruritus commonly induce clinical signs of hair loss, scaling, scales piercing hairs, odor, and/or greasy seborrhea. Marked pedal pruritus and facial rubbing are common in animals with concurrent yeast and bacterial infections. Before pursuing allergies as a cause of pruritus or performing skin biopsies or other more expensive and/or invasive diagnostic testing, a concurrent bacterial and yeast infection should be ruled out. A 21–30 day concurrent course of an antibiotic effective against Staphylococcus spp (eg, cephalexin 30 mg/kg, PO, bid) and a systemic antifungal (eg, ketoconazole, itraconazole, or fluconazole 5–10 mg/kg, PO, sid) should be prescribed. If the pruritus resolves, then existing pruritus was due to a microbial infection.

It is possible that the initial trigger is long gone or seasonal. However, if the animal's pruritus is unchanged or only somewhat better, the most likely underlying cause is allergic (assuming parasitic causes have been ruled out). The most common causes of allergic pruritus are insect bite hypersensitivity (eg, flea allergy, mosquito bite allergy, fly bite), food allergy, and atopic dermatitis. Flea allergy dermatitis and insect bite hypersensitivity are ruled out based on response to insect control. Animals that do not have insect bite hypersensitivity but are seasonally pruritic most likely have atopic dermatitis. Animals with year-round allergic pruritus have atopic dermatitis and/or food allergy. Food allergy is ruled in or out based on response to a diet trial and provocative challenge. Atopic dermatitis is a clinical diagnosis; in vitro allergy testing and intradermal skin testing show only antigen exposure patterns. These tests are used to determine the contents of an immunotherapy vaccine.

Treatment

Successful therapy depends on identification of the underlying cause. Patients with idiopathic pruritus or those in which treatment of the underlying disease does not eliminate the pruritus (eg, atopic patients) will require medical management of pruritus.

Antihistamines

The efficacy of antihistamines for the treatment of pruritus is suspect based on evidence-based medicine reports. The most commonly used antihistamines include hydroxyzine hydrochloride (2.2 mg/kg, PO, tid), diphenhydramine (2.2 mg/kg, PO, bid), amitriptyline hydrochloride (2.2 mg, PO, bid), cetirizine (5 mg/cat or 5–10 mg/dog, sid or bid), and fexofenadine (2–3 mg/kg, PO, sid or bid). A 7–10 day therapeutic trial of any one antihistamine is required to see maximal benefit.

Essential Fatty Acids

Essential fatty acids are rarely effective as sole antipruritic agents; however, they often act synergistically with antihistamines and/or glucocorticoids. They may enhance the effectiveness of antihistamines or allow a small dose of glucocorticoids to be used. The exact doses are unknown, but the current recommendation is 180 mg eicosapentaenoic acid/5 kg, PO, sid-bid.

Glucocorticoids

Glucocorticoids are the most effective drugs in the management of pruritus. However, they cannot be used safely for longterm management due to adverse effects (eg, suppression of adrenal function, risk of development of diabetes mellitus, risk of secondary urinary tract infections). In addition, owners can rarely tolerate the common side effects (polydipsia, polyuria, polyphagia, and panting) for long periods of time. Anti-inflammatory dosages range from 0.5–1.0 mg/kg, PO, sid for 5–10 days and then every other day. Topical spray formulations of triamcinolone acetate are highly effective and good alternatives to oral steroids.

Other Systemic Antipruritic Agents

Other effective agents include cyclosporine 5 mg/kg, PO, sid), pentoxifylline (10–25 mg/kg, PO, bid-tid), and misoprostol (3–6 μg/kg, PO, tid). Of these, cyclosporine A modified is the most effective and is used for the treatment of allergies in dogs. It has been used to treat many cats successfully as well, although not FDA-approved for use in this species. It is initially given 1 or more times per day until allergy symptoms are controlled, then the dose may be reduced. It takes ~2 wk for improvement to become evident, and as long as 4–6 wk for maximal effects. The most common adverse effects are nausea, anorexia, vomiting, loose stools, and diarrhea. These usually resolve after several weeks.

Last full review/revision July 2011 by Karen A. Moriello, DVM, DACVD