Difference between revisions of "Equine Serum Hepatitis"
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| − | == | + | {| cellpadding="10" cellspacing="0" border="1" |
| + | | Also known as: | ||
| + | | '''Theiler's disease<br> | ||
| + | |} | ||
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| + | ==Description== | ||
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| + | Equins Serum Hepatitis (ESH) leading to acute liver failure is most commonly associated with prior administration of an equine biologic product. This is most commonly tetanus antitoxin, but encephalitis vaccines and equine serum have also been implicated. Other possible hypotheses include alkaloid toxicity and mycotoxins. Several cases have been reported in which no biologic product had been administered, leading to the possibility that an infectious agent may be involved. | ||
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==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 | + | 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. |
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==Clinical Signs== | ==Clinical Signs== | ||
| − | The | + | The history may include administration of an equine-derived biologic product, often four to six weeks prior to the onset of clinical signs. They are generally sudden in onset and rapidly progressive. |
| − | Signs may range from mild | + | Signs may range from mild lethargy or inappetance to signs of acute or chronic hepatic failure. They may be non-specific such as depression, anorexia or weight loss. Affected horses are often severely icteric and may pass dark urine due to the presence of bilirubin. Signs relating to hepatic encephalopathy may be present such as head pressing, apparent blindness, yawning or aimless wandering. Dermatological signs such as photosensitisation or pruritus may also be seen. The course of the disease is usually around five days, with death ususally occuring within ten days. |
Mild forms of the disease have also been reported, characterised by a mild malaise and increased serum hepatic enzyme concentrations. | Mild forms of the disease have also been reported, characterised by a mild malaise and increased serum hepatic enzyme concentrations. | ||
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==Diagnosis== | ==Diagnosis== | ||
| − | Diagnosis of ESH and evaluation of hepatic function may be achieved using | + | Diagnosis of ESH and evaluation of hepatic function may be achieved using three types of diagnostic test. Serum biochemistry may indicate the following abnormalities: |
| − | |||
* Increased conjugated and unconjugated bilirubin | * Increased conjugated and unconjugated bilirubin | ||
* Increased liver enzymes- SDH, AST, GGT and ALP | * Increased liver enzymes- SDH, AST, GGT and ALP | ||
* Hypoglycaemia | * Hypoglycaemia | ||
| − | * | + | * Reduced urea |
| − | + | Bilirubinuria may also be present. | |
| − | + | In several studies, biopsy is considered as the ‘gold standard’ technique for hepatic disease diagnosis. 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. | |
| − | |||
| − | + | ==Pathology== | |
| − | + | Post mortem examination often shows the liver to be enlarged and pale with rounded edges. Generalised icterus is often present. Histologically there may signs of acute hepatocellular degeneration. be 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== | |
| − | + | 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. If the horse is still able to eat, a low protein, high carbohydrate diet should be fed. The protein should be high in branched-chain amino acids, and corn and molasses are often used to achieve this. | |
| − | + | ==Prognosis== | |
| − | + | The prognosis for horses with signs of hepatic encephalopathy is extremely poor with a mortality rate approaching 100%. Horses that survive for a week after the onset of clinical signs may recover. A fall in SDH is associated with a better prognosis. | |
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==References== | ==References== | ||
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| − | + | [[Category:Liver_-_Inflammatory_Pathology]][[Category:Horse]] | |
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| − | [[Category:Liver_-_Inflammatory_Pathology]] | ||
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| − | [[Category: | + | [[Category:To_Do_-_SophieIgnarski]] |
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Revision as of 12:05, 24 July 2010
| Also known as: | Theiler's disease |
Description
Equins Serum Hepatitis (ESH) leading to acute liver failure is most commonly associated with prior administration of an equine biologic product. This is most commonly tetanus antitoxin, but encephalitis vaccines and equine serum have also been implicated. Other possible hypotheses include alkaloid toxicity and mycotoxins. Several cases have been reported in which no biologic product had been administered, leading to the possibility that an infectious agent may be involved.
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.
Clinical Signs
The history may include administration of an equine-derived biologic product, often four to six weeks prior to the onset of clinical signs. They are generally sudden in onset and rapidly progressive.
Signs may range from mild lethargy or inappetance to signs of acute or chronic hepatic failure. They may be non-specific such as depression, anorexia or weight loss. Affected horses are often severely icteric and may pass dark urine due to the presence of bilirubin. Signs relating to hepatic encephalopathy may be present such as head pressing, apparent blindness, yawning or aimless wandering. Dermatological signs such as photosensitisation or pruritus may also be seen. The course of the disease is usually around five days, with death ususally occuring within ten days.
Mild forms of the disease have also been reported, characterised by a mild malaise and increased serum hepatic enzyme concentrations.
Diagnosis
Diagnosis of ESH and evaluation of hepatic function may be achieved using three types of diagnostic test. Serum biochemistry may indicate the following abnormalities:
- Increased conjugated and unconjugated bilirubin
- Increased liver enzymes- SDH, AST, GGT and ALP
- Hypoglycaemia
- Reduced urea
Bilirubinuria may also be present.
In several studies, biopsy is considered as the ‘gold standard’ technique for hepatic disease diagnosis. 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.
Pathology
Post mortem examination often shows the liver to be enlarged and pale with rounded edges. Generalised icterus is often present. Histologically there may signs of acute hepatocellular degeneration. be 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
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. If the horse is still able to eat, a low protein, high carbohydrate diet should be fed. The protein should be high in branched-chain amino acids, and corn and molasses are often used to achieve this.
Prognosis
The prognosis for horses with signs of hepatic encephalopathy is extremely poor with a mortality rate approaching 100%. Horses that survive for a week after the onset of clinical signs may recover. A fall in SDH is associated with a better prognosis.
References
- Edward Robinson, N and Sprayberry, K. A. (2009) Current Therapy In Equine Medicine Sixth edition Saunders Elsevier
- Knottenbelt, D.C. A Handbook of Equine Medicine for Final Year Students University of Liverpool
- Lavoie, J. P., Hinchcliff, K. W. (2009) Blackwell's Five-Minute Veterinary Consult: Equine Wiley-Blackwell
- Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial
- Smith, H. L., Chalmers, G. A., Wedel, R. (1991) Acute hepatic failure (Theiler's disease) in a horse Canadian Veterinary Journal 32, 362-364.