Page 1019 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
P. 1019

994                                        CHAPTER 8



  VetBooks.ir  Electrocardiography results are variable,   ranging   overload and cellular damage or death. Acutely, this
                                                          may result in cell dysfunction. Over time, myode-
           from no abnormalities to premature ventricu-
           lar  contractions and  ventricular tachycardia.
           Echocardiography may be unremarkable, although   generation, loss of myocytes and replacement with
                                                          fibrosis may occur. Decreased cardiac function may
           a reduction in ventricular function may be present.  result. Additionally, arrhythmias are potentiated due
                                                          to regional variation in signal conduction and block-
           Management                                     age, resulting in aberrant conduction.
           Underlying disease should be diagnosed and treated
           if possible. Supportive therapy is indicated. This  Clinical presentation
           may include anti-inflammatory therapy with flu-  Clinical signs are variable and dependent in part on
           nixin meglumine (0.5–1.0 mg/kg i/v or p/o q12 h) or   the extent and duration of exposure to toxins. Signs
           dexamethasone (0.05–0.2 mg/kg i/v or i/m q24 h).   range from mild depression to sudden death. Ataxia,
           Corticosteroids should be administered with caution   weakness, intermittent profuse sweating, difficulty
           if active viral infection is suspected. Broad-spectrum   rising and eventual recumbency are common in
           antimicrobials may be of benefit if bacterial infection   acute toxicity. Congestive heart failure, tachycar-
           is suspected. Strict stall rest is indicated to limit car-  dia and arrhythmias have been documented. Severe
           diac workload. This period of rest should continue   dyspnoea relating to either cardiogenic pulmonary
           until clinical signs have resolved. Horses should be   oedema or diaphragm failure may occur. Death in
           re-examined prior to return to any form of exer-  acute cases occurs within 24–48 hours of exposure.
           cise because of the risk of syncope associated with   Hepatic, renal and skeletal muscle abnormalities
           arrhythmias. Exercise intolerance may persist due to   may also be present. The onset of clinical signs may
           myocardial damage.                             occur immediately post exposure but can be delayed
                                                          for weeks. Delayed signs may occur in horses that
           TOXIC MYOCARDITIS                              recover from the acute phase or have experienced
                                                          subacute or chronic low-level exposure. Subacute
           Definition/overview                            signs include depression, cardiac arrhythmia, tachy-
           The most commonly reported cause for toxin-induced   cardia and heart failure. Poor performance may be a
           myocardial disease in horses is exposure to ionophores.   result of acute intoxication and may be the sole clini-
           Ionophores are antibiotics that facilitate the move-  cal sign.
           ment of cations across biological membranes. These
           agents are used as growth promoters in cattle feeds  Differential diagnosis
           and as  coccidiostats in poultry feeds. Horses are exqui-  Viral myocarditis, cantharidin toxicosis, idiopathic
           sitely sensitive to ionophores and exposure to minute   cardiomyopathy and vitamin D toxicosis may pro-
           amounts can cause clinical signs. The LD50s for   duce similar signs.
           salinomycin, monensin and lasalocid are 0.6 mg/kg,
           2–3 mg/kg and 21.5 mg/kg, respectively, in horses.  Diagnosis
           Cantharidin (blister beetle) toxicosis and exposure   Toxin-associated disease should be suspected when
           to plants containing cardiac glycosides (e.g. oleander,   multiple animals are affected. Recent feeding of
           milkweed, foxglove) may also cause similar signs.  a  new  source  or  new  shipment  of  feed  should  be
                                                          queried and, if present, provides further suspicion.
           Aetiology/pathophysiology                      The feed should be inspected, and samples saved.
           Toxic insults to the myocardium may result in acute   Failure of several animals to consume feeds should
           cellular necrosis, leading to fibrosis. The mechanism   also prompt investigation of the feed. Definitive
           of action of the toxins is variable. Ionophores damage   diagnosis is based on detection within the feed of
           cells  by altering cation  distribution across the cell   ionophores or cardiac glycosides or the detection of
           membrane. Facilitation of movement of cations such   blister beetles within the hay. Gastric content analy-
           as calcium into the cardiac cell may result in calcium   sis is important in animals that die suddenly.
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