Page 815 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
P. 815

790                                        CHAPTER 4



  VetBooks.ir  flutter, muscle fasciculation and weakness may be   be administered until the horse has been rehydrated.
                                                          Analgesics  may  be  required.  Supplementation  of
           present  as  a  result  of  hypocalcaemia.  Sometimes,
           horses may have a stiff gait suggestive of acute myo-
                                                          be required and is ideally based on repeated evalu-
           sitis. Sudden death occurs in some cases.      intravenous fluids with calcium borogluconate may
                                                          ation of serum calcium levels. Magnesium supple-
           Differential diagnosis                         mentation is less commonly required. Sucralfate
           Other causes of GI, urinary and systemic disease   (20 mg/kg p/o q6–8 h) may be useful if gastritis
           must be considered, depending on the clinical   or EGUS has developed. Administration of broad-
           presentation.                                  spectrum antimicrobials is frequently recommended
                                                          based on concerns of bacterial translocation from
           Diagnosis                                      affected  intestine;  however,  there  is  little  evidence
           Clinical and laboratory findings are non-specific.   to support this concern. Nephrotoxic antimicrobials
           A history of eating alfalfa hay or other alfalfa prod-  such as aminoglycosides should be avoided.
           ucts supports the suspicion in endemic regions.   Treatment of other potentially exposed horses with
           Identification of blister beetles in hay is highly sug-  mineral oil or activated charcoal may be indicated.
           gestive; however, a failure to identify blister beetles
           does not rule out the disease. The PCV is usually  Prognosis
           elevated. Total protein level is usually normal or ele-  The prognosis depends on the amount of toxin
           vated initially, but hypoproteinaemia may develop   ingested and the severity of disease at the time of treat-
           over time. Neutrophilia may be present as may hypo-  ment but is poor overall. Early and aggressive treat-
           calcaemia, hyperglycaemia and hypomagnesaemia.   ment is required. Persistent tachycardia, tachypnoea
           Serum urea and creatinine levels may be elevated,   and elevated CK levels are poor prognostic indicators.
           and urinalysis should be performed to  differentiate
           pre-renal from renal disease. Hyposthenuria may  SPASMODIC COLIC
           be present for unknown reasons in some cases.
           Microscopic haematuria will be evident early in the  Definition/overview
           disease, with gross haematuria occurring later. An   Spasmodic colic is probably the most common type
           elevation in creatine kinase (CK) may be present in   of colic in adult horses.
           severely affected animals and may indicate a poorer
           prognosis. Oesophageal and gastric inflammation or  Aetiology/pathophysiology
           ulceration may be evident endoscopically.      The specific aetiology is unclear. An association
             Cantharidin can be identified in urine or intesti-  between  Anoplocephala perfoliata  (tapeworm) infes-
           nal contents in the first few days of disease; however,   tation and spasmodic colic has been reported, and
           availability of testing may be limited. Urine (mini-  changes in diet and a history of recent anthelmintic
           mum 500 ml) or gastric contents (minimum 200 g)   administration are important risk factors. Individual
           should be submitted.                           horses may be predisposed to recurrent spasmodic
                                                          colic for unknown reasons.
           Management                                       Abnormal contractions, or spasms, of the intes-
           There is no antidote. Supportive therapy is essential.   tine may result in the development of abdominal pain
           The hay source should be changed to prevent further   through stimulation of stretch receptors. Intestinal
           intoxication. Removal of recently ingested canthari-  spasms are transient and do not result in intestinal
           din may be attempted via administration of mineral   obstruction.
           oil (4–6 litres per NG tube) or activated charcoal (1–3
           g/kg per NG tube). Intravenous fluid therapy with a  Clinical presentation
           balanced electrolyte solution should be commenced.   Affected horses usually display signs of mild to
           Administration of diuretics (furosemide, 1 mg/kg     moderate abdominal pain, including anorexia, roll-
           i/v or i/m q6 h) has been recommended to increase   ing, flank-watching, kicking at the abdomen, pawing,
           cantharidin excretion; however, diuretics should not   recumbency and straining to urinate or defaecate.
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