Changes

==Signalment==

==Signalment==

ESH occurs predominantly in older horses. Cases (both individual cases and outbreaks) occur relatively frequently during the autumn months in north western USA, however some parts of the world have no reported cases. Some reports suggest that lactating broodmares given tetanus antitoxin after parturition are particularly prone to Theiler's disease.

ESH occurs predominantly in older horses. Cases (both individual cases and outbreaks) occur relatively frequently during the autumn months in north western USA, however some parts of the world have no reported cases. Some reports suggest that lactating broodmares given tetanus antitoxin after parturition are particularly prone to ESH.

==Clinical Signs==

==Clinical Signs==

Diagnosis of ESH and evaluation of hepatic function may be achieved using a combination of clinical history, abrupt onset of clinical signs and diagnostic tests indicative of hepatic insufficiency. Serum biochemistry may indicate the following abnormalities:

Diagnosis of ESH and evaluation of hepatic function may be achieved using a combination of clinical history, abrupt onset of clinical signs and diagnostic tests indicative of hepatic insufficiency. Serum biochemistry may indicate the following abnormalities:

* Increased conjugated and unconjugated bilirubin

* Increased conjugated and unconjugated bilirubin

* Increased urea

* Increased urea

Ultrasound may reveal a smaller than normal liver with a loss of parenchymal structure and enlarged bile ducts. In several studies, biopsy is considered as the ‘gold standard’ technique for definitive diagnosis of hepatic disease. Biopsy is usually performed on the right hand side, between the twelth and fourteenth intercostal spaces. A coagulation profile is often performed prior to performing the procedure.  

 

Ultrasound may reveal a smaller than normal liver with a loss of parenchymal structure and enlarged bile ducts. In several studies, biopsy is considered as the ‘gold standard’ technique for definitive diagnosis of hepatic disease. Biopsy is usually performed on the right hand side between the twelth and fourteenth intercostal spaces. A coagulation profile is often performed prior to performing the procedure.  

==Pathology==

==Pathology==

Post mortem examination often shows generalised icterus and ascites, with an enlarged and pale liver. Histologically there may signs of acute hepatocellular degeneration including centrilobular to midzonal necrosis with mononuclear cell accumulation within the portal triads. Contusions, lacerations or fractures may be present if the disease has had a violent clinical course.  

Post mortem examination often shows generalised icterus and ascites, with an enlarged and pale liver. Histologically there may be signs of acute hepatocellular degeneration including centrilobular to midzonal necrosis, with mononuclear cell accumulation within the portal triads. Contusions, lacerations or fractures may be present if the disease has had a violent clinical course.  

==Treatment==

==Treatment==

The aims of treatment are mainly to support liver function until hepatic compromise can occur. Affected horses should be housed in a quiet, darkened stable in order to minimise stimulation. Sedation may be required if signs of hepatic encephalopathy are present. Stressful situations such as moving the horse or separating it from field mates should be avoided.

The aims of treatment are mainly to support liver function until hepatic compromise can occur. Affected horses should be housed in a quiet, darkened stable in order to minimise stimulation. Sedation may be required if signs of hepatic encephalopathy are present. Stressful situations such as moving the horse or separation from field mates should be avoided.

If the horse is still able to eat, a low protein, high carbohydrate diet should be fed. In order to reduce the severity of neurological signs, the protein should be high in branched-chain amino acids; corn and molasses are often used to achieve this. If the horse is anorexic, a naso-gastric tube can be passed and high energy foods given directly into the stomach.

If the horse is still able to eat, a low protein, high carbohydrate diet should be fed. In order to reduce the severity of neurological signs, the protein should be high in branched-chain amino acids; corn and molasses are often used to achieve this. If the horse is anorexic, a naso-gastric tube can be passed and high energy foods given directly into the stomach.