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hemorrhage,  platelet  counts  are typically  higher   transfusion with clotting factors alone (i.e. a plasma-
            than immune-mediated cases (often 50,000–    containing product without red blood cells) is indi-
  VetBooks.ir  150,000/hpf). Regardless if immune-mediated   cated. Typically, fresh frozen plasma (plasma frozen
                                                         for  <1  year)  or  frozen  plasma  (plasma  frozen  for
            destruction or consumption of platelets secondary
            to another disease is suspected, it is important to
                                                         neither of these products have functional platelets.
            try to diagnose the underlying condition to stop the   >1–3 years) can be used in these cases. Note that
            destruction.  This usually involves a systemic   Also, frozen plasma may contain lesser amounts of
            workup including testing for tick-borne (Rickettsial)   factors  V  and  VIII  than fresh frozen plasma
            diseases, imaging of the thorax and abdomen look-  depending on duration of storage, and therefore
            ing for underlying neoplasia or other disease, and   may be more limited in its efficacy.
            potentially performing a bone marrow biopsy to   Once hemorrhage is controlled and any anemia
            evaluate the megakaryocytes and other platelet   is corrected, more diagnostic tests can be con-
            precursors. While attempting to look for the under-  ducted to look for the underlying cause of the dis-
            lying disease, both primary and secondary immune-  order. The first step is often to look critically at the
            mediated destruction is controlled by administration   degree of PT prolongation versus aPTT prolonga-
            of immunosuppressive drugs including steroids,   tion to try to narrow down the possible etiologies.
            cyclosporine, mycophenolate mofetil, and azathio-  See Table 9.2 for an approach to evaluating the PT
            prine. Further treatments to apprehend the immune   and aPTT. Subsequently, further diagnostics might
            system (intravenous immunoglobulin) or stimulate   include testing for specific clotting factors, investi-
            megakaryocyte platelet release (vincristine) can   gation into possible anticoagulant rodenticide
            also be attempted. In many cases, while test results   exposure, or evaluation of liver function.  The
            for Rickettsial disease are pending, animals are also   reader is referred to the Further Reading section for
            prophylactically treated with doxycycline.  The   more information on evaluating specific clotting
            reader is referred to the Further Reading section for   factors and liver function. Longer term treatment
            more information on the specific treatments for   and outcomes for these cases are dependent upon
            ITP. If another underlying disease is diagnosed that   the underlying cause. For example, a case of antico-
            is causing platelet consumption, platelet counts   agulant  rodenticide  intoxication  can be  treated
            should improve once that disease is addressed.  with vitamin K supplementation until the toxin is
                                                         cleared from the body (1–6 weeks depending on
                                                         the product ingested). In contrast, liver functional
            Secondary hemostatic disorders
                                                         failure needs to be managed long term and may not
            Secondary hemostatic disorders have only limited   be reversible.
            treatment  options,  which  are again  somewhat
            dependent upon the cause of the clotting factor
            disorder. As with platelet disorders, the first clinical   9.5  Pitfalls of the Monitor
            decision is whether or not the animal requires   All laboratory testing is subject to various causes
            emergent treatment to stop bleeding. This is argu-  for error. Please see Box 9.1 for a summary of the
            ably more important in secondary coagulation   most common reasons for alterations in the typical
            disorders than primary disorders since secondary   coagulation tests. Further detail related to each of
            disorders often involve larger volumes of hemor-  the reasons listed in Box 9.1 is found in the text
            rhage than primary disorders.                within this section.
              If an animal is clinical for either anemia (typically
            packed  cell volume  <12–15%) or  hypovolemia
            (tachycardia, weak peripheral pulses, obtundation,   Primary hemostasis
            pale mucous membranes), it requires emergent
            transfusion of plasma with functional clotting fac-  Platelet counts
            tors as well as red blood cells.  Typically, whole   When interpreting platelet counts, the most common
            blood or multicomponent therapy (packed red   spurious finding is a pseudothrombocytopenia that
            blood cells AND fresh frozen plasma) is indicated in   occurs secondary to platelet clumping. Attention to
            these cases. Otherwise, if the animal has prolonga-  atraumatic venipuncture, gentle sample  handling,
            tions of coagulation tests (e.g. prolonged PT, aPTT,   and reducing the delay in placing the blood in an
            or ACT) without severe anemia or hypovolemia,   anticoagulant may help reduce   clumping. Despite


             192                                                         E.J. Thomovsky and A.C. Brooks
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