Difference between revisions of "Hyperlipaemia - Horse"
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| − | Do not confuse with: [[Hyperlipidaemia - Horse|'''Hyperlipidaemia<br>]] | + | {| cellpadding="10" cellspacing="0" border="1" |
| + | | Also known as: | ||
| + | | '''Fatty liver syndrome<br> | ||
| + | |-} | ||
| + | | Do not confuse with: | ||
| + | | [[Hyperlipidaemia- Horse|'''Hyperlipidaemia<br>]] | ||
| + | |-} | ||
| − | == | + | ==Description== |
'''Hyperlipaemia''' is a severe metabolic disorder which occurs in response to a negative energy balance, the end result is multi-organ failure as lipid is deposited in the liver and kidneys. Fatty acids are mobilised from adipose tissue, some are used peripherally but most are taken up by the liver. Here they are oxidized to provide energy or re-esterified to triglycerides and phospholipids, and deposited in hepatocytes or released into the blood as very low density lipoproteins. These very low density lipoproteins are the cause of lipaemic plasma in hyperlipaemic ponies. Hypoglycaemia reduces insulin response, compounding the problem by increasing peripheral lipid mobilisation and decreasing removal of triglyercides from the circulating blood. Insulin resistance has been reported to be a factor in many cases of hyperlipaemia but affected animals may aslo have a normal insulin response. | '''Hyperlipaemia''' is a severe metabolic disorder which occurs in response to a negative energy balance, the end result is multi-organ failure as lipid is deposited in the liver and kidneys. Fatty acids are mobilised from adipose tissue, some are used peripherally but most are taken up by the liver. Here they are oxidized to provide energy or re-esterified to triglycerides and phospholipids, and deposited in hepatocytes or released into the blood as very low density lipoproteins. These very low density lipoproteins are the cause of lipaemic plasma in hyperlipaemic ponies. Hypoglycaemia reduces insulin response, compounding the problem by increasing peripheral lipid mobilisation and decreasing removal of triglyercides from the circulating blood. Insulin resistance has been reported to be a factor in many cases of hyperlipaemia but affected animals may aslo have a normal insulin response. | ||
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==Signalment== | ==Signalment== | ||
| − | Occurs most commonly in '''Shetland''' and '''miniture ponies''' but has also been reported in horses; it is also relatively common in [[Hyperlipaemia - | + | Occurs most commonly in '''Shetland''' and '''miniture ponies''' but has also been reported in horses; it is also relatively common in [[Hyperlipaemia- Donkeys|donkeys]] and follows the same pathogenesis. |
Affected animals are usually but not consistently obese and the condition occurs in animals which are in a negative energy balance, most frequently due to pregnancy, lactation, [[Colic in Horses|colic]] or chronic disease. | Affected animals are usually but not consistently obese and the condition occurs in animals which are in a negative energy balance, most frequently due to pregnancy, lactation, [[Colic in Horses|colic]] or chronic disease. | ||
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==Treatment== | ==Treatment== | ||
Treatment must be prompt and aggressive. | Treatment must be prompt and aggressive. | ||
| − | Nutritional support is the most important part of treatment. Constant slow infusion of glucose IV ( | + | Nutritional support is the most important part of treatment. Constant slow infusion of glucose IV (dexrose 5%)should be given initially. Followed by protamine zinc insulin (15IU/kg IM q12h) and glucose (0.5g/kg PO q 12h) or high energy gruel based on barley or oats given by stomach tube and supportive amino acids. Heparin (40-100 IU/kg SC q12h) may be given in an attempt to reduce plasma triglyerides but will not correct the underlying cause and may alter haemostasis. |
==Prognosis== | ==Prognosis== | ||
Prognosis is poor. | Prognosis is poor. | ||
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==References== | ==References== | ||
* Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''' ''University of Liverpool'' | * Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students''' ''University of Liverpool'' | ||
| − | *Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition) | + | *Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition) Sauders. |
| − | + | [[Category:Liver_-_Degenerative_Pathology]][[Category:Horse]] | |
| − | + | [[Category:To_Do_-_lizzyk]] | |
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| − | [[Category:Liver_-_Degenerative_Pathology]][[Category: | ||
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Revision as of 17:24, 23 July 2010
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This article is still under construction. |
Description
Hyperlipaemia is a severe metabolic disorder which occurs in response to a negative energy balance, the end result is multi-organ failure as lipid is deposited in the liver and kidneys. Fatty acids are mobilised from adipose tissue, some are used peripherally but most are taken up by the liver. Here they are oxidized to provide energy or re-esterified to triglycerides and phospholipids, and deposited in hepatocytes or released into the blood as very low density lipoproteins. These very low density lipoproteins are the cause of lipaemic plasma in hyperlipaemic ponies. Hypoglycaemia reduces insulin response, compounding the problem by increasing peripheral lipid mobilisation and decreasing removal of triglyercides from the circulating blood. Insulin resistance has been reported to be a factor in many cases of hyperlipaemia but affected animals may aslo have a normal insulin response.
Metabolic acidosis can occur in the terminal stages of the disease and is a poor prognostic indicator. Secondary laminitis is a common complicating factor.
Signalment
Occurs most commonly in Shetland and miniture ponies but has also been reported in horses; it is also relatively common in donkeys and follows the same pathogenesis.
Affected animals are usually but not consistently obese and the condition occurs in animals which are in a negative energy balance, most frequently due to pregnancy, lactation, colic or chronic disease.
Diagnosis
Visual inspection of plasma is usually sufficient to diagnose the condition, in affected animals the serum will be turbid and cloudy with elevated triglyceride concertrations (5.7mmol/L). Liver enzymes, bilirubin and bile acid concentrations are often elevated and there may be a concurrent azotaemia.
Clinical Signs
- Depression
- Anorexia
- Ataxia
- Diarrhoea
- Peripheral oedema
Biochemistry
- Elevated liver enzymes, AST AP GGT
- Elevated bile acids
- Hypoglycaemia
- Hypoalbuminaemia
- Azoteamia
Pathology
Liver biopsy shows fatty infiltration of hepatocytes.
Post mortem exam reveals lipaemic serum, and a pale enlarged friable liver with a greasy surface when cut.
Treatment
Treatment must be prompt and aggressive. Nutritional support is the most important part of treatment. Constant slow infusion of glucose IV (dexrose 5%)should be given initially. Followed by protamine zinc insulin (15IU/kg IM q12h) and glucose (0.5g/kg PO q 12h) or high energy gruel based on barley or oats given by stomach tube and supportive amino acids. Heparin (40-100 IU/kg SC q12h) may be given in an attempt to reduce plasma triglyerides but will not correct the underlying cause and may alter haemostasis.
Prognosis
Prognosis is poor.
References
- Knottenbelt, D.C. A Handbook of Equine Medicine for Final Year Students University of Liverpool
- Rose, R. J. and Hodgson, D. R. (2000) Manual of Equine Practice (Second Edition) Sauders.
| Also known as: | Fatty liver syndrome |
| Do not confuse with: | Hyperlipidaemia |