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It has been surveyed that, although horses appear to be a strong energy force, they are in fact most sensitive to human emotion and illness. Horse lovers describe riding as "an emotion in motion" in support of the above statement.
If horses are not cared for in a tentative manner they tend to show the signs of it very quickly. Horse diseases can therefore also include personal growth elements. NLP is a form of language used for both the horse and carer or rider. It is a short term for "Neuro Linguistic Programming". An interpersonal communication model and alternative to psychotherapy, based on the subjective study of language, communication and personal change.
Like humans, a disease, sickness or wound on the outer parts of a horses body can have deeper route causes other than the most obvious symptoms for illnesses such as white line disease, hoof rot, mange, horse sickness and lameness to name a few. It may be the horses immune system is run down causing vulnerability to disease. It may also be the horses emotional state whilst interacting with the rider or carer which can induce vulnerability to illness.
Either way, caring for the emotional and psychological needs of a horse are as important as nurturing a proud flesh wound with a topical solution.
Liver disease in horse :clinical signs and diagnostic aids
The clinical signs of hepatic insufficiency in horses are highly variable, nonspecific and depend on the extent and duration of hepatic disease.
The most common clinical signs are weight loss, hepatic encephalopathy, icterus and colic. Rarely reported clinical signs of hepatic insufficiency in horses are ascites, dependent abdominal edema, endotoxic shock and hemolysis.
Significant weight loss and failure to thrive are most consistently present during chronic hepatic insufficiency. However, chronic liver disease may be present without apparent weight loss.
Behavioral manifestations
The earliest phase of HE manifests as subtle behavioral changes. As it progresses, there may be signs of depression, head-pressing, circling, mild ataxia, aimless walking, persistent yawning and other inappropriate behavior (Photo 1). In advanced cases, somnolence develops and obtunded behavior ensues. At this stage horses often show aggressive or violent behavior interspersed with the periods of stupor. The severity of encephalopathy corresponds to the degree of hepatic dysfunction; however, neither of these parameters correlates with type or reversibility of the underlying hepatic disease.
The diagnosis of HE is based on the presence of signs of cerebral dysfunction, with physical examination and laboratory findings compatible with liver disease.
Jaundice
When hepatocellular disease or obstruction to bile flow is present, icterus develops as a consequence of impaired conjugation of bilirubin and impeded excretion of conjugated bilirubin into the biliary tract, respectively
The presence of icterus is not specific to liver disease. About 10 percent of healthy horses have slightly yellow sclerae and horses that are anorexic for any reason will develop icterus. Intense icterus also develops subsequent to hemolysis.
Finally, certain drugs (steroids, heparin) can impede bilirubin uptake and conjugation by hepatocytes, despite an otherwise normally functioning liver.
Abdominal pain or colic may be a result of acute hepatic swelling or pressure from obstruction of bile flow. Interestingly, many horses with liver disease and signs of colic have clinically significant gastric impactions


Light sensitivity
Hepatic photosensitization refers to abnormally heightened reactivity of the skin to ultraviolet sunlight, owing to the increased blood concentration of the photodynamic agent phylloerythrin. Phylloerythrin normally is formed in the gastrointestinal tract as a result of bacterial degradation of chlorophyll. During hepatic insufficiency, the blood concentrations of phylloerythrin are increased. Ultraviolet light is absorbed most efficiently in unpigmented areas; thus the lesions of photosensitization are restricted to white skin which first appears erythematous and edematous. Pruritus, pain, vesiculation, ulceration, necrosis and sloughing may ensue (Photo 2

Diarrhea and hemostasis
Diarrhea may infrequently accompany chronic hepatic insufficiency in horses. Alterations in the intestinal microflora, portal hypertension and deficiency of bile acids may be involved in the pathogenesis.
Because the liver is responsible for the synthesis of numerous factors involved in coagulation, abnormal hemostasis may be a sequela to hepatic insufficiency. Clinical signs may vary from ecchymotic hemorrhages, to hemorrhage after trauma or venipuncture, to spontaneous hemorrhage (Photo 2).
Although not common, a fever may be present in horses with hepatic abscesses, acute hepatitis, chronic active hepatitis, obstructive cholelithiasis, fatty liver failure or neoplasia.
Intravascular hemolysis is a rarely seen, but grave prognostic indicator of fulminate hepatic failure in horses. Hypoalbuminemia and water retention can occur with chronic liver failure and may result in dependent edema. Because the half-life of albumin is relatively long in the horse, edema is a rare clinical sign. Dependent abdominal edema may form if there is significant portal hypertension and ascites.
Failure of Kupffer-cell phagocytosis of endotoxin may result in clinical and laboratory evidence of endotoxemia
Laboratory findings of hepatic insufficiency
Because massive hepatic disease must be present before alterations are seen with some laboratory tests, and because different liver functions are variably altered by disease, the laboratory diagnosis of hepatic disease can be challenging.
The most useful diagnostic tests for evaluation of hepatic disease in horses are quantitation of sorbitol dehydrogenase (SDH) and gamma-glutamyl transpeptidase or -transferase (GGT) activity and serum bile acids concentration (SBA).
Although increases in SDH, GGT and SBA are highly specific for liver disease, they are not specific for the type of disease.
Sorbitol dehydrogenase (SDH) has been widely used in the evaluation of acute liver disease in horses. Some clinicians consider GGT the test of highest sensitivity in evaluating horses for liver disease. Increases are more persistent in chronic disease, especially with cholestasis. The normal liver removes greater than 90 percent of bile acids from the enterohepatic circulation. Thus, the blood concentration of bile acids may be increased with liver disease and quantitation provides an excellent screen of liver function.
Increased serum bile acid concentrations are highly specific for the presence of liver disease (may increase within 24 to 48 hours after the onset of hepatic disease), but are not specific for the type of liver disease.
A value less than 20 micromolel/L appears to be a good predictor in ruling out significant functional liver disease and should be included in the evaluation of horses suspected to have hepatic disease. Bile acid concentrations are highest in biliary obstructive diseases and portosystemic shunts.
Other cytosolic liver enzymes include aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LD) and alanine aminotransferase (ALT).

Other nonspecific tests
Additional nonspecific tests of liver disease in the horse include quantitation of bilirubin, albumin, globulins, ammonia, BUN, coagulation proteins, glucose and esterified triglycerides.
Serum bilirubin concentration is not a sensitive indicator of liver disease in horses, as hemolysis, anorexia and the administration of certain drugs will increase the unconjugated bilirubin concentration.
An increase in the conjugated bilirubin fraction is more reliably indicative of hepatic disease in horses than is the unconjugated bilirubin concentration. When the conjugated bilirubin concentration is greater than 25 percent of the total bilirubin value, hepatocellular disease should be suspected. If the conjugated bilirubin concentration is greater than 30 percent of the total value, cholestasis should be suspected.
In normal horses, the total bilirubin concentration is in the range of 0.2 to 5.0 mg/dL, with conjugated bilirubin in the range of 0 to 0.4 mg/dL. Plasma cells respond to the general increased antigen load, resulting in polyclonal gammopathy.
Because the liver primarily is responsible for removing ammonia from circulation and converting it to urea for renal excretion, increases in the blood ammonia concentration or a decrease in the blood urea nitrogen (BUN) concentration (<9 mg/dL) may be indicative of chronic hepatocellular disease. Typically, a 50 percent to 70 percent decrease in the blood concentration of the coagulation factors is necessary before a change in these clotting time-based assays is detectable.
Changes in the blood-glucose concentration are rarely seen in horses with liver insufficiency. The concentration of blood triglycerides may become increased during hepatic insufficiency as a result of increased mobilization from adipose tissue to support energy-requiring processes, coupled with decreased clearance by the liver