Page 944 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
P. 944

Endocrine system                                      919



  VetBooks.ir  factors include stress, malnutrition and intestinal   observance of lipaemic plasma. Liver enzymes and
                                                         function tests should be measured in cases of hyper-
          parasitism.
            Negative energy balance results in activation of
          hormone-sensitive lipase and mobilisation of glycerol,   lipaemia. Additional testing to identify possible
                                                         inciting causes should be undertaken.
          free fatty acids (FFAs), and non-esterified fatty acids
          (NEFAs) from adipose tissue. These nutrients travel  Management
          in the blood to the liver, where they can be converted   The two primary goals of treatment are (1) to identify
          to  glucose  by  gluconeogenesis  or  oxidised  to  acetyl-  and treat the inciting cause of the negative energy
          CoA. Fatty acids can also be converted to ketones,   balance or the underlying disease, and (2) to improve
          and in many species, ketosis is an important result of   the energy balance. Depending on the severity of the
          fat mobilisation. This does not occur to a significant   hyperlipaemia, improving the energy balance may
          degree  in  horses  because  they  have  efficient  ketone   be as simple as offering palatable feeds to encour-
          transport into the mitochondria, where they can be   age eating. Administration of NSAIDs may improve
          processed into energy via the TCA cycle. The large   appetite in horses with high fevers or who are in pain.
          volume of FFAs that are mobilised from the adipose   Provision of a higher energy diet or force-feeding via
          tissue are both re-esterified to triglycerides and very   nasogastric tube may also be effective in mild cases.
          low-density phospholipids and  accumulate in the hepa-  Preparations that can be administered by nasogas-
          tocytes, which leads to fatty liver. The peripheral tis-  tric tube include solutions of glucose (or dextrose)
          sues cannot use the phospholipids as quickly as the liver   and electrolytes, gruels made from pelleted feeds or
          produces them, leading to increased blood concentra-  commercially available enteral solutions. Improperly
          tions of triglycerides and grossly lipaemic serum.  balanced home-made solutions  containing  glucose
                                                         and electrolytes may exacerbate metabolic acidosis
          Clinical presentation                          or result in hyperglycaemia. Commercially available
          Clinical signs include anorexia, depression and weak-  enteral solutions are convenient but may be cost pro-
          ness, progressing to muscle fasciculations, ataxia,   hibitive except in smaller equids. Gruels made from
          head pressing, circling, recumbency and convulsions   complete pelleted feeds have the advantage that they
          or coma. Ventral oedema may be present. Diarrhoea   are nutritionally complete and relatively inexpensive,
          may accompany the syndrome, either as an inciting   but they require coadministration of a large volume
          cause of the negative energy balance or secondary to   of water to keep the gruel from clogging the tube.
          anorexia. Parasitism may contribute to poor appetite   This large volume makes it necessary to administer
          and compete for nutrients.                     multiple meals (usually a minimum of six) through-
                                                         out the day, in order to satisfy dietary requirements
          Differential diagnosis                         without overloading the stomach. It is usually neces-
          The primary clinical signs of anorexia, depression   sary to start with a smaller amount of feed (e.g. 50%)
          and weakness are non-specific and can be caused   on the first day and gradually increase the amount
          by many diseases. Often, hyperlipaemia occurs sec-  given per feeding over a few days until either 100%
          ondary  to  another  disease  process  and  the  initial   of the required diet is reached or the horse begins
          clinical signs of hyperlipidaemia are either missed   eating voluntarily.
          or ascribed to the original problem. Primary dif-  Moderate cases of hyperlipaemia may require i/v
          ferentials for anorexia should include fever or GI   infusion of glucose (5 or 10%) and/or force-feeding
          problems including, but not limited to, colic, gastric   by nasogastric tube. Concurrent administration of
          ulcers and colitis. Differential diagnoses for the diar-  a balanced electrolyte solution is required to pro-
          rhoea include the various causes of colitis.   vide maintenance fluid requirements and account
                                                         for any ongoing losses (i.e. diarrhoea). Fluid ther-
          Diagnosis                                      apy is particularly important in azotaemic ani-
          Diagnosis is made by measurement of elevated tri-  mals. Frequent monitoring of blood glucose levels
          glycerides (>6.65 mmol/l [500 mg/dl]) in plasma or   should be performed to help maintain a steady level.
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