Page 1378 - Small Animal Internal Medicine, 6th Edition
P. 1378

1350   PART XIII   Hematology


            exogenous corticosteroids may result in decreased antibody   phosphate (1-2 mg/kg). I also advocate the use of prophylac-
            binding to the surface of the RBCs.                  tic heparin and/or aspirin therapy because dogs with hemo-
  VetBooks.ir  to 2-4 mg/kg of prednisone q12-24h) constitute the treat-  lysis are at high risk for DIC and thrombosis. I use heparin
              Immunosuppressive doses of corticosteroids (equivalent
                                                                 therapy, 50 to 75 IU/kg subcutaneously (SC) q8h, and/or
            ment of choice for primary IHA. Although dexamethasone
            can be used initially, it should not be used as maintenance   minidose aspirin, 0.5 mg/kg PO q24h. These dosages of
                                                                 heparin usually do not result in therapy-related prolongation
            therapy for prolonged periods because of its higher potential   of the activated clotting time (ACT) or activated partial
            to cause GI tract ulceration or pancreatitis; in addition, if
            given on an alternate-day basis, it causes interference with
            the hypothalamic-pituitary-adrenal axis. In equivalent doses,      Prednisone
            dexamethasone does not appear to be more beneficial than   30                              800
            prednisone in dogs. In cats with IHA, I use dexamethasone           Cytoxan
            (4-5 mg/cat PO q1-2 wk) instead of prednisolone, with a                 Transfusion
            high degree of success.                                                                    600
              A high percentage of dogs treated with corticoster-      20
            oids show a marked improvement within 24 to 96 hours
            (Fig. 82.7). Corticosteroids mainly act by three different                                 400
            mechanisms—they suppress MPS activity, decrease comple-   PCV (%)                                Platelets (×1000/µL)
            ment  and  antibody  binding  to  the  cells,  and  suppress  Ig
            production. The first two effects are rapid in onset (hours),   10
            whereas the third effect is delayed (1-3 weeks). For addi-                                 200
            tional information, see Chapters 72 and 73.
              I have seen a high number of dogs with acute or peracute
            IHA generally associated with icterus and autoagglutination   0                            0
            that undergo rapid deterioration and usually die of throm-   0      2     4     6      8
            boembolism of the liver, lungs, or kidneys despite aggressive              Day
            corticosteroid therapy (Fig. 82.8). In those patients, I use   FIG 82.7
            cyclophosphamide (Cytoxan), 200 to 300 mg/m  PO or IV   Response to treatment in a dog with immune hemolytic
                                                   2
            in a single dose over a 5- to 10-minute period, or human IV   anemia (IHA) and immune-mediated thrombocytopenia
            immunoglobulin (IVIG), 0.5 g/kg as an IV infusion, in con-  (Evans syndrome). PCV, Packed cell volume; –•–, PCV;
            junction with a single IV dose of dexamethasone sodium   –Δ–, platelets; ↓, treatment administered.
















                                                           L                                          L











                    A                                          B

                          FIG 82.8
                          Thoracic radiographs before (A) and after anticoagulant therapy (B) in a mixed-breed
                          dog with immune hemolytic anemia (IHA). Notice the almost complete consolidation of the
                          left pulmonary field (A) and resolution 72 hours after treatment with heparin and aspirin
                          (B).
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