Page 1140 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
P. 1140

Nervous system                                      1115



  VetBooks.ir  gradual reduction of serum sodium over a few days,   protein bound, especially to albumin, and 10% com-
                                                         plexed  with  anions  such  as  citrate  and  phosphate.
          along with supportive care and treatment of the
                                                         Only ionised calcium is biologically active and there-
          cerebral oedema.
                                                         fore the measurement of ionised calcium is more
          HYPOCALCAEMIA                                  clinically relevant. Acid–base status should also be
                                                         determined because alkalosis decreases ionised cal-
          Definition/overview                            cium levels, while acidosis increases the ionised cal-
          Hypocalcaemia  is a  relatively uncommon  cause  of   cium level. The protein-bound fraction will decrease
          weakness in the horse (see also p. 910).       with hypoalbuminaemia and therefore a low total
                                                         calcium concentration, secondary to hypoalbumi-
          Aetiology/pathophysiology                      naemia, is usually clinically irrelevant because the
          Hypocalcaemia in horses may occur in a number of   ionised calcium concentration remains normal.
          situations. Lactation tetany in mares, transit tetany
          associated with transportation over long distances,  Management
          idiopathic hypocalcaemia, exhausted horse  syn-  This condition can be life-threatening and war-
          drome associated with endurance competitions, sep-  rants immediate treatment in most cases. Treatment
          sis/endotoxaemia, malabsorption syndromes, renal   involves  the  administration  of  intravenous  cal-
          disease, severe rhabdomyolysis and other causes   cium solutions such as 20% calcium borogluconate
          including cantharidin toxicosis have been reported.  (0.25–1.0 ml/kg of 23% calcium gluconate slowly i/v
                                                         diluted 1:4 with saline or dextrose). Administration
          Clinical presentation                          should be closely monitored via the cardiovascular
          Clinical signs are similar to those seen with tetanus   response. The infusion should be suspended, or the
          and are due to increased skeletal muscle and cardiac   rate decreased, if signs of cardiotoxicity (bradycardia
          muscle excitability. Signs include a stiff gait, muscle   or arrhythmias) develop. Resolution of clinical signs
          fasciculations, trismus, dysphagia, pyrexia, tachycar-  can occur within minutes to hours of calcium infu-
          dia, sweating, cardiac dysrhythmias, seizures, coma   sion. High calcium forages, such as alfalfa, should be
          and death. Synchronous diaphragmatic flutter is a   fed to horses with recurrent hypocalcaemia.
          sign  that  is  also  frequently  associated  with  hypo-
          calcaemia (but can also occur with other electrolyte  Prognosis
          abnormalities) and is thought to occur as a result of   The prognosis depends on the ability to correct the
          altered membrane potential of the phrenic nerve,   underlying condition. Idiopathic hypocalcaemia in
          which passes directly over the atrium, resulting in   foals carries a poor prognosis.
          nerve discharges in response to atrial depolarisation.
          The severity of clinical signs is usually proportional  NEOPLASIA OF NERVOUS TISSUE
          to the degree of hypocalcaemia. Total calcium values
          of 1.25–2.0 mmol/l (5–8 mg/dl) may produce tetanic   With the exception of pituitary adenoma, neoplasia
          spasms, while values of below 1.25 mmol/l (5 mg/dl)   of the CNS is extremely rare in horses. Only non-
          result in recumbency and stupor.               pituitary CNS neoplasms will be discussed in this
                                                         section.
          Diagnosis                                        The prevalence of equine neurological disease
          Diagnosis is based on the recognition of character-  related to neoplasms has been estimated at 2%, with
          istic clinical signs in affected horses combined with   tumours of lymphoid origin being the most com-
          laboratory demonstration of hypocalcaemia. Other   mon. Primary neoplasms of the nervous system
          abnormalities that can be seen in association with   are very rare, and in a survey of North American
          hypocalcaemia are metabolic alkalosis, hyper/hypo-  university  veterinary  hospitals,  all  nervous  tissue
          magnesaemia, and hypo/hyperphosphataemia. Total   tumours found in horses involved peripheral nerves.
          serum calcium is approximately 50% ionised, 40%   Neurofibromas and neurofibrosarcomas were the
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