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300  Section 4  Respiratory Disease

              Identifying  the  allergens  responsible  for inciting  the   Albuterol sulfate is a beta‐2‐adrenergic agonist that
  VetBooks.ir  asthmatic response in individual cats is a critical step in   may be administered in inhalant form to cats presenting
                                                              with severe, acute dyspnea. A metered dose inhaler is
            devising targeted therapies. Methods have been devel-
            oped to detect IgE that is specific for the allergens used
                                                              attached  to a facemask  (Aerokat® Feline  Aerosol
            in sensitization in the serum of cats with experimentally   used to deliver the medication into a chamber device
            induced asthma. Moreover, intradermal skin testing, a   Chamber, Trudell Medical International). This appara-
            practice most often used in the diagnosis of atopic   tus facilitates inhalation of the aerosolized particles into
              dermatitis, has been shown to be a sensitive means of   the lower airways. An initial dose of one 90 μg puff can
            detecting aeroallergen sensitization in experimental   be administered to dyspneic patients that will tolerate
            models of asthma. Other minimally invasive immunodi-  having the facemask held over the nose and mouth for
            agnostic methods that have been investigated in asth-  the 7–10 seconds necessary for the complete dose to be
            matic patients include the use of flow cytometry to   inhaled. This dose may be repeated every 30 minutes for
            detect  proliferation of allergen‐specific T lymphocytes in   up to four hours. Albuterol can also be dispensed for
            the peripheral blood.                             at‐home administration as a “rescue inhaler” for man-
                                                              agement of acute exacerbations in established asthmat-
                                                              ics until veterinary care can be provided. However,
              Treatment                                       chronic use of racemic albuterol should be avoided as
                                                              the S‐enantiomer in this mixture has been shown to
            Supplemental oxygen, stress reduction, and bron-  cause airway inflammation in healthy and experimen-
            chodilation are the tenets of therapy for the asthmatic   tally asthmatic cats.
            cat in acute crisis. For the patient presenting with   Status asthmaticus is defined in human medicine as
            dyspnea and cyanosis, supplemental oxygen should be   severe, acute asthma that is refractory to repeated doses
            provided immediately at a FiO 2  of 40%. This can be   of beta‐agonists. Severely dyspneic feline asthmatics that
            effectively  accomplished  by  placing  the  patient  in  an   do  not respond to bronchodilators and  supplemental
            oxygen cage, which also minimizes restraint and han-  oxygen may stabilize only after initiating antiinflamma-
            dling that can exacerbate dyspnea, with fatal outcomes   tory therapy with a rapidly acting glucocorticoid such as
            in some instances.                                dexamethasone sodium phosphate. An initial dose of
              Beta‐2‐adrenergic agonists such as terbutaline are   0.25–2 mg/kg can be administered IM or IV to quickly
            most commonly used to induce bronchodilation in an   reduce airway inflammation if necessary.
            acute setting. Bronchodilation results from airway   Lifelong glucocorticoid therapy is the key to chronic
            smooth muscle relaxation triggered by stimulation of   management of feline asthma. Because the aeroallergen
            beta‐2‐adrenergic receptors. Activation of these recep-  that provokes the asthmatic response usually cannot be
            tors triggers adenylyl cyclase to increase production of   identified or completely removed, avoidance of the
            cAMP, which sequesters intracellular calcium, thereby   offending allergen is often impossible in feline patients.
            reducing smooth muscle contraction. Other potentially   Thus, it is postulated that lower airway inflammation is
            beneficial effects of these agents include inhibition of   continually present in asthmatic cats, even in the absence
            mast cell mediator release and airway microvascular   of clinical signs. Lower airway inflammation has been
            leakage, increased mucociliary clearance, decreased   shown to persist in feline asthmatics treated with high‐
            neutrophil activation and endothelial adhesion, and   dose glucocorticoid therapy despite resolution of clinical
            induction of neutrophil apoptosis. Adverse effects asso-  signs. To minimize the permanent airway remodeling
            ciated  with  beta‐2‐adrenergic  agonist  therapy  include   that ensues from long‐standing inflammation, continu-
            tachycardia, CNS stimulation, hypokalemia, and trem-  ous antiinflammatory therapy is necessary.
            ors. For this reason, these agents should be used with   Glucocorticoids are the most effective antiinflamma-
            caution in patients with co‐morbid cardiac disease,   tory agents used in the management of feline asthma.
            hypertension, hyperthyroidism, seizure disorders, and   They exert their antiinflammatory effects by binding to a
            diabetes mellitus. Beta‐2‐adrenergic agonists can inter-  cytosolic receptor, then translocating to the nucleus
            act with tricyclic antidepressants such as amitriptyline   where the glucocorticoid–receptor complex binds to a
            and clomipramine and should be used with caution in   glucocorticoid response element on the genes that regu-
            patients receiving these medications. Terbutaline sul-  late production of inflammatory cytokines such as IL‐3
            fate  can be administered IM or SC at an initial dose   and IL‐5. Glucocorticoids also increase vasoconstriction
            of  0.1 mg/kg to induce bronchodilation in an acute   to reduce airway edema; decrease airway hyperrespon-
              setting.  Decreased respiratory rate is expected within    siveness over time; decrease mucus secretion; inhibit
            15–30 minutes of dosing, and repeated doses can be   macrophages, T cells, eosinophils, and mast cells;
            administered as needed.                           increase the synthesis of secretory leukocyte protease
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