Page 1048 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
P. 1048

H aemolymphatic system                                   1023



  VetBooks.ir  iron cacodylate (1 g/adult horse) should be given   mechanisms are suspected, but the lesion is limited to
                                                         developing erythrocytes. With recombinant human
          slowly. Iron dextran should not be administered
          because of the high incidence of adverse reactions,
                                                         develops to the foreign protein, which cross-reacts
          including anaphylaxis and death. Iron should   erythropoietin administration, an immune response
          not be administered to foals in the first 2 days of   and removes both administered and endogenous
          life. PCV should be monitored 1–3 times weekly   erythropoietin.
          during initial treatment. Serum iron and TIBC
          should be evaluated every 2 weeks. Iron supple-  Clinical presentation
          mentation can be ceased when serum iron, TIBC   In AA the animal is initially presented with pete-
          and PCV are within reference intervals. Weeks of   chial haemorrhages and epistaxis, or intermittent
          supplementation may be required in severely iron-  fever and weight loss, reflecting loss of platelets
          depleted animals.                              and neutrophils, respectively. In PRCA the anae-
                                                         mia is usually moderate to severe and animals
          Prognosis                                      develop pallor, weakness, decreased exercise toler-
          The prognosis is good if the reason for the iron   ance and lethargy.
          depletion can be discovered and eliminated.
                                                         Differential diagnosis
          APLASTIC ANAEMIA AND                           Other causes of pancytopenia or non-regenerative
          PURE RED CELL APLASIA                          anaemia, including iron deficiency and AID, should
                                                         be considered, although the latter tend to be less
          Definition/overview                            severe.
          Aplastic anaemia (AA) is a bone marrow stem-
          cell disorder characterised by decreased produc-  Diagnosis
          tion of all blood cell types and replacement of   Diagnosis  is made  by documenting  haemato-
          normal haematopoietic tissue with adipose tissue.   logical abnormalities (pancytopenia with AA
          Pure red cell aplasia (PRCA) is characterised by a   and non-regenerative anaemia with PRCA) on
          severe  non-regenerative anaemia due to a deple-  repeated CBCs, and examination of bone marrow
          tion of developing erythrocytic precursors in the   demonstrating marked hypoplasia to aplasia and
          bone marrow. Leucocytes and platelets tend to be   replacement with adipose tissue (AA) or severely
          unaffected in PRCA. These diseases occur rarely   decreased or absent developing erythrocytic pre-
          in the horse.                                  cursors (PRCA) (Figs. 9.25, 9.26).

          Aetiology/pathophysiology                      Management
          The inciting cause is often unknown, but immune-  If an underlying disease process can be documented,
          mediated phenomena and idiosyncratic drug reac-  appropriate therapy should be administered.
          tion should be considered. Most cases are idiopathic.   Otherwise, supportive care, administration of broad-
          Administration of recombinant human erythropoi-  spectrum antibiotics and blood product transfusions
          etin has also been reported to result in PRCA in   are appropriate. Bone marrow transplantation could
          horses.                                        provide a cure but has not been evaluated and is not
            In AA it is suspected that immune-mediated   available for horses.
          mechanisms are induced subsequent to exposure to
          an infectious agent or drug. It is thought that anti-  Prognosis
          bodies develop to unknown antigens on the sur-  The prognosis for AA or PRCA is generally guarded
          face  of  developing  stem  cells  in the  bone marrow,   to poor, but there may be a response to immunosup-
          and these cells are removed, resulting in lack of   pressive therapy. Recovery may take several weeks
          production of mature cell types. In PRCA, similar   to months.
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