Difference between revisions of "Hepatic Encephalopathy - Horse"
| (8 intermediate revisions by 2 users not shown) | |||
| Line 1: | Line 1: | ||
| − | {{ | + | {{unfinished}} |
| − | == | + | ==Description== |
| − | '''Hepatic encephalopathy''' is neurological | + | '''Hepatic encephalopathy''' is neurological disfunction caused by any acute or severe hepatic damage; 60-80% of hepatic function must be lost before clinical signs develop. |
| − | + | A combination of the following mechanisms are probably responsible for the syndrome, hepatic insufficiency allows the build up of ammonia which affects neurotransmission in the CNS, toxic metabolites may act as false neurotransmitters and there can be an imblance between excitatory and inhibitory neurotransmission. | |
==Signalment== | ==Signalment== | ||
| − | No age, sex or breed | + | No age, sex or breed predisposions. |
| − | There are many hepatic disorders which can lead to hepatic encephalopathy including, '''Hepatitis, [[Ragwort Toxicity]], [[Tyzzer's Disease]]''' and '''[[Hyperlipaemia - Horse|Hyperlipaemia]]''' | + | There are many hepatic disorders which can lead to hepatic encephalopathy including, '''[[Hepatitis, Equine Serum|Hepatitis]], [[Ragwort Toxicity]], [[Tyzzer's Disease]]''' and '''[[Hyperlipaemia - Horse|Hyperlipaemia]]''' |
==Diagnosis== | ==Diagnosis== | ||
| − | |||
| − | |||
===Clinical Signs=== | ===Clinical Signs=== | ||
| − | Clinical signs vary depending on the severity of hepatic dysfunction, and may be associated with feeding. | + | Clinical signs vary depending on the severity of hepatic dysfunction, early signs are often subtle and may be missed. Clinical signs may be associated with feeding. |
Four clinical stages have been described for hepatic encephalopathy: | Four clinical stages have been described for hepatic encephalopathy: | ||
* Stage I: Mild changes in mentation; this stage is usually missed in horses. | * Stage I: Mild changes in mentation; this stage is usually missed in horses. | ||
* Stage II: Depressed mental state, lethargy, behavioural changes, head pressing, ataxia and dysphagia. | * Stage II: Depressed mental state, lethargy, behavioural changes, head pressing, ataxia and dysphagia. | ||
| − | * Stage III: Somnolent but rousable. Reactions may be very reduced or | + | * Stage III: Somnolent but rousable. Reactions may be very reduced or exagerrated. |
* Stage IV: Coma, Seizures are rare but may occur in the late stages of the condition. | * Stage IV: Coma, Seizures are rare but may occur in the late stages of the condition. | ||
| Line 31: | Line 29: | ||
===Biopsy=== | ===Biopsy=== | ||
| − | A liver biopsy can provide a definitive diagnosis of liver disease | + | A liver biopsy can provide a definitive diagnosis of liver disease, a clotting profile should be carried out before taking an ultrasound-guided biopsy. |
===Ultrasound=== | ===Ultrasound=== | ||
| Line 37: | Line 35: | ||
===Pathology=== | ===Pathology=== | ||
| − | See [[Hepatic Encephalopathy | + | See [[Hepatic Encephalopathy]] Pathology |
==Treatment== | ==Treatment== | ||
| − | With | + | With supportive therapy horses may recover from hepatic encephalopathy after 4-21 days. Treatment is only warranted in acute cases likely to make a recovery. |
| − | '''Sedation''' is often necessary in cases of hepatic encephalopathy; An alpha 2 agonist at a low dose is usually effective. If the neurological signs are so severe that the horse is a danger to itself and others then ''' | + | '''Sedation''' is often necessary in cases of hepatic encephalopathy; An alpha 2 agonist at a low dose is usually effective. If the neurological signs are so severe that the horse is a danger to itself and others then immediate '''euthansia''' is indicated. |
| − | Fluid deficits and acid base abnormalities should be corrected as necessary and hypoglycaemic animals should be given a 5% dextrose solution IV. High carbohydrate, low protein diets should be fed in small amounts and frequently | + | Fluid deficits and acid base abnormalities should be corrected as necessary and hypoglycaemic animals should be given a 5% dextrose solution IV. High carbohydrate, low protein diets should be fed in small amounts and frequently. |
| − | |||
| − | |||
==Prognosis== | ==Prognosis== | ||
| − | Prognosis is '''poor''' to severe but | + | Prognosis is '''poor''' to severe but depend on the underlying disease; signs are potentially reversible if the initiating course can be corrected. |
| − | Horses with hepatic disease showing neurological signs have a poorer prognosis than those showing only signs | + | Horses with hepatic disease showing neurological signs have a poorer prognosis than those showing only signs af hepatic dysfunction. However with appropriate supportive therapy 40% of horses survive for at least 6 months. Recovery may be incomplete and temporary. |
| − | |||
| − | |||
| − | |||
| − | |||
==References== | ==References== | ||
| Line 65: | Line 57: | ||
* Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition) Sauders. | * Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition) Sauders. | ||
| − | + | [[Category:To_Do_-_lizzyk]] | |
| − | + | [[Category:Liver_Disorders_-_Horse]] | |
| − | + | [[Category:Neurological_Disorders_-_Horse]] | |
| − | |||
| − | |||
| − | [[ | ||
| − | [[Category: | ||
| − | [[Category: | ||
Revision as of 14:08, 19 August 2010
 |
This article is still under construction. |
Description
Hepatic encephalopathy is neurological disfunction caused by any acute or severe hepatic damage; 60-80% of hepatic function must be lost before clinical signs develop.
A combination of the following mechanisms are probably responsible for the syndrome, hepatic insufficiency allows the build up of ammonia which affects neurotransmission in the CNS, toxic metabolites may act as false neurotransmitters and there can be an imblance between excitatory and inhibitory neurotransmission.
Signalment
No age, sex or breed predisposions.
There are many hepatic disorders which can lead to hepatic encephalopathy including, Hepatitis, Ragwort Toxicity, Tyzzer's Disease and Hyperlipaemia
Diagnosis
Clinical Signs
Clinical signs vary depending on the severity of hepatic dysfunction, early signs are often subtle and may be missed. Clinical signs may be associated with feeding.
Four clinical stages have been described for hepatic encephalopathy:
- Stage I: Mild changes in mentation; this stage is usually missed in horses.
- Stage II: Depressed mental state, lethargy, behavioural changes, head pressing, ataxia and dysphagia.
- Stage III: Somnolent but rousable. Reactions may be very reduced or exagerrated.
- Stage IV: Coma, Seizures are rare but may occur in the late stages of the condition.
Additional clinical signs associated with hepatic disease:
- Weight loss
- Diarrhoea
- Icterus
Laboratory Tests
Haemotology and Biochemistry results will be consistent with hepatic disease; including increased GGT and SDH, hypoalbuminaemia and elevated bile acids.
Biopsy
A liver biopsy can provide a definitive diagnosis of liver disease, a clotting profile should be carried out before taking an ultrasound-guided biopsy.
Ultrasound
Transabodimal ultrasound can be used to assess the structure of the liver and degree of damage.
Pathology
See Hepatic Encephalopathy Pathology
Treatment
With supportive therapy horses may recover from hepatic encephalopathy after 4-21 days. Treatment is only warranted in acute cases likely to make a recovery.
Sedation is often necessary in cases of hepatic encephalopathy; An alpha 2 agonist at a low dose is usually effective. If the neurological signs are so severe that the horse is a danger to itself and others then immediate euthansia is indicated.
Fluid deficits and acid base abnormalities should be corrected as necessary and hypoglycaemic animals should be given a 5% dextrose solution IV. High carbohydrate, low protein diets should be fed in small amounts and frequently.
Prognosis
Prognosis is poor to severe but depend on the underlying disease; signs are potentially reversible if the initiating course can be corrected. Horses with hepatic disease showing neurological signs have a poorer prognosis than those showing only signs af hepatic dysfunction. However with appropriate supportive therapy 40% of horses survive for at least 6 months. Recovery may be incomplete and temporary.
References
- Bertone, J. (2006) Equine Geriactric Medicine and Surgery, Elsevier
- Brown, C.M, Bertone, J.J. (2002) The 5-Minute Veterinary Consult- Equine', Lippincott, Williams & Wilkins
- Knottenbelt, D.C. A Handbook of Equine Medicine for Final Year Students University of Liverpool
- Mair, T., Love, S., Schumacher, J. and Watson, E. (1998) Equine Medicine, Surgery and Reproduction WB Saunders Company Ltd
- Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial
- Reed, S.M, Bayly, W.M, Sellon, D.C. (2004) Equine Internal Medicine (Second Edition) Saunders.
- Rose, R. J. and Hodgson, D. R. (2000) Manual of Equine Practice (Second Edition) Sauders.