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Abnormal behavior

Horses with abnormal behavior often act obtunded or maniacal, with compulsive movements and seeming disPicture 2: This photo demonregard to their safety or the welfare of others. Abnormal strates early signs behavior generally implies dysfunction of the forebrain, of botulism, includthough brainstem disease can also cause obtundation to ing weak tongue tone and failure to stupor. Common causes of abnormal behavior include retract tongue into metabolic encephalopathies, EPM, and head trauma. Viral the mouth. encephalitides are common causes in certain regions, Image Credit: although less so for horses with appropriate vaccination Dr. Robert H. histories. Whitlock The two most common metabolic encephalopathies in horses are “intestinal encephalopathy,” or hyperammonemia associated with intestinal dysfunction, and hepatic encephalopathy. Signs of metabolic encephalopathy include central blindness, bizarre behavior, compulsive walking, obtunded or stuporous mental status, seizures, and mild ataxia. Forebrain (prosencephalic) signs generally predominate. Additionally, horses with intestinal encephalopathy often show signs of colic or diarrhea prior to developing neurologic signs. Diagnosis of intestinal encephalopathy and supportive evidence for hepatic encephalopathy requires accurate measurement of ammonia in blood or CSF, which is often difficult in field settings. Identification of a laboratory that can perform blood ammonia testing (as well as clarification Horses with altered behavior due to EPM are treated of ideal sample storage and handling) in advance of needing this service is advantageous. Clinically affected horses similarly to horses with spinal ataxia due to EPM, but often have levels over 200 µmol/L, although neurologic the overall prognosis is worse,5 and relapses seem to be signs have been observed with levels as low as 60 µmol/L.3 If more common. Note on head trauma: There is a limited amount of inforhepatic dysfunction is present, liver enzyme activities (AST, SDH, GGT, ALP), as well as indicators of hepatic function mation on equine traumatic brain injury, but one retrospec(bilirubin, bile acids), are likely to be increased. Metabolic tive study6 suggests that the most common clinical signs are ataxia, nystagmus, abnormal mental status, abnormal (lactic) acidosis and hyperglycemia are common findings. Emergency treatment for hyperammonemia or hepatic pupils (size, symmetry, or PLRs), and head tilt. Poll injury encephalopathy should focus on minimizing trauma sec- from falling over backwards was more common than frontal ondary to bizarre behavior, restoring adequate hydration injury. In this study of 34 horses, the survival rate was 62%. and acid-base status, and neuroprotection.4 Most horses Prolonged recumbency (> 4 four hrs after admission) and require sedation to be handled safely and to prevent basilar skull bone fractures were risk factors for nonsurpatient-induced trauma. Intermittent doses of detomidine vival. The most important principles for managing head (10-20 µg/kg IV) or a CRI of detomidine (5-20 µg/kg/hr) trauma include maintenance of adequate brain oxygenare recommended. If available and not cost-prohibitive, ation and perfusion, which requires careful attention to phenobarbital (5-10 mg/kg IV) can be used to prolong respiratory and circulatory status. Hypotension is a wellsedation or reduce seizure activity. Intravenous fluids with established predictor of death in people with traumatic supplemental KCl (20-40 mEq/L) are invariably required. brain injury, so intravenous fluids should be administered Hypertonic saline (2-4 mL/kg) or mannitol (0.5 – 1 g/kg) to restore circulating volume. Reduction of cerebral edema can be administered to reduce cerebral edema, which might (if present) will improve brain perfusion and overall neuor might not be part of the pathogenesis. Either lactulose rologic function. In a field setting, hypertonic saline (2-4 (0.2 – 0.3 mL/kg q 6-12h) or neomycin (20 mg/kg q 12-24) mL/kg), followed by isotonic crystalloid fluid administracan be administered orally or via nasogastric intubation to tion is the easiest way to accomplish both of these goals. If there are open wounds or fractures, broad-spectrum reduce ammonia absorption or production. Prognosis is guarded to fair for intestinal encephalopa- antimicrobial treatment should be initiated. Anti-fungal thy; reported survival in one retrospective study was 39%.3 treatment should be considered based on region and locaIn the author’s experience, horses that recover usually do tion of wounds. Whether steroid treatment is beneficial for so quickly, with significant improvement in six to 24 hours, affected horses remains unclear; steroid treatment is no and horses that do not recover often die or require euthana- longer recommended for people with traumatic brain injury, sia in the same time period. Prognosis is guarded for hepatic as the most recent meta-analysis7 showed an increase in encephalopathy as the inciting hepatic problem is often mortality with steroid use. - Continued on page 20 irreversible. WWW.FAEP.NET |

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Practitioner Issue 4, 2017  

A publication by the Florida Association of Equine Practitioners, an equine-exclusive division of the FVMA. Your Invitation to Attend the Oc...

Practitioner Issue 4, 2017  

A publication by the Florida Association of Equine Practitioners, an equine-exclusive division of the FVMA. Your Invitation to Attend the Oc...

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