Difference between revisions of "Hepatic Encephalopathy - Horse"
(11 intermediate revisions by 2 users not shown) | |||
Line 1: | Line 1: | ||
− | {{ | + | {{OpenPagesTop}} |
− | == | + | ==Introduction== |
− | '''Hepatic encephalopathy''' is neurological | + | '''Hepatic encephalopathy''' is neurological dysfunction caused by any acute or severe hepatic damage; 60-80% of hepatic function must be lost before clinical signs develop. |
+ | |||
+ | The cause of hepatic encephalopathy is hepatic insufficiency; the pathophysiology causing the neurological dysfunction is probably multifactorial. The following mechanisms have been suggested: accumulation of gastro-intestinal derived neurotoxins, imbalance of inhibitory and excitatory neurotransmitters, disruption of CNS energy metabolism, and the development of false neurotransmitters. | ||
==Signalment== | ==Signalment== | ||
− | No age, sex or breed | + | No age, sex or breed predispositions. |
− | There are many hepatic disorders which can lead to hepatic encephalopathy including, ''' | + | There are many hepatic disorders which can lead to hepatic encephalopathy including, '''Hepatitis, [[Ragwort Toxicity]], [[Tyzzer's Disease]]''' and '''[[Hyperlipaemia - Horse|Hyperlipaemia]]''' |
==Diagnosis== | ==Diagnosis== | ||
+ | Diagnosis is made on clinical signs of cerebral dysfunction with evidence of hepatic insufficiency, in the absence of other potential causes for the neurological signs. | ||
+ | |||
===Clinical Signs=== | ===Clinical Signs=== | ||
− | Clinical signs vary depending on the severity of hepatic dysfunction, | + | Clinical signs vary depending on the severity of hepatic dysfunction, and 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 | + | * 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 exaggerated. |
− | * Stage IV: Coma, Seizures | + | * Stage IV: Coma, Seizures are rare but may occur in the late stages of the condition. |
− | |||
Additional clinical signs associated with hepatic disease: | Additional clinical signs associated with hepatic disease: | ||
Line 28: | Line 31: | ||
===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 34: | Line 37: | ||
===Pathology=== | ===Pathology=== | ||
− | See [[Hepatic Encephalopathy]] | + | See [[Hepatic Encephalopathy#Pathology|hepatic encephalopathy pathology]] |
==Treatment== | ==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. | + | 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 '''euthanasia''' may be 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 | + | 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. |
+ | |||
+ | Lactulose, mineral oil and neomycin or metronidazole can be administered in an attempt to reduce the production and absorption of hepatic toxins. | ||
==Prognosis== | ==Prognosis== | ||
− | Prognosis is '''poor''' to severe but | + | Prognosis is '''poor''' to severe but depends 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 of hepatic dysfunction. However with appropriate supportive therapy 40% of horses survive for at least 6 months. Recovery may be incomplete and temporary. |
+ | |||
+ | {{Learning | ||
+ | |literature search = [http://www.cabdirect.org/search.html?q=%28title%3A%28Hepatic%29+OR+title%3A%28liver%29+OR+title%3A%28Portosystemic%29%29+AND+%28title%3A%28Encephalopathy%29+OR+title%3A%28coma%29%29+AND+od%3A%28horses%29 Hepatic Encephalopathy in horses publications] | ||
+ | }} | ||
==References== | ==References== | ||
Line 53: | Line 62: | ||
* Mair, T., Love, S., Schumacher, J. and Watson, E. (1998) '''Equine Medicine, Surgery and Reproduction''' ''WB Saunders Company Ltd'' | * 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'' | * 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. | * Rose, R. J. and Hodgson, D. R. (2000) '''Manual of Equine Practice''' (Second Edition) Sauders. | ||
− | [[ | + | |
− | [[Category: | + | {{review}} |
− | [[Category: | + | |
+ | {{OpenPages}} | ||
+ | |||
+ | [[category:Expert_Review]] | ||
+ | [[Category:Liver Diseases - Horse]] | ||
+ | [[Category:Neurological Diseases - Horse]] |
Latest revision as of 18:52, 6 July 2012
Introduction
Hepatic encephalopathy is neurological dysfunction caused by any acute or severe hepatic damage; 60-80% of hepatic function must be lost before clinical signs develop.
The cause of hepatic encephalopathy is hepatic insufficiency; the pathophysiology causing the neurological dysfunction is probably multifactorial. The following mechanisms have been suggested: accumulation of gastro-intestinal derived neurotoxins, imbalance of inhibitory and excitatory neurotransmitters, disruption of CNS energy metabolism, and the development of false neurotransmitters.
Signalment
No age, sex or breed predispositions.
There are many hepatic disorders which can lead to hepatic encephalopathy including, Hepatitis, Ragwort Toxicity, Tyzzer's Disease and Hyperlipaemia
Diagnosis
Diagnosis is made on clinical signs of cerebral dysfunction with evidence of hepatic insufficiency, in the absence of other potential causes for the neurological signs.
Clinical Signs
Clinical signs vary depending on the severity of hepatic dysfunction, and 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 exaggerated.
- 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 euthanasia may be 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.
Lactulose, mineral oil and neomycin or metronidazole can be administered in an attempt to reduce the production and absorption of hepatic toxins.
Prognosis
Prognosis is poor to severe but depends 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 of hepatic dysfunction. However with appropriate supportive therapy 40% of horses survive for at least 6 months. Recovery may be incomplete and temporary.
Hepatic Encephalopathy - Horse Learning Resources | |
---|---|
Literature Search Search for recent publications via CAB Abstract (CABI log in required) |
Hepatic Encephalopathy in horses publications |
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.
This article has been peer reviewed but is awaiting expert review. If you would like to help with this, please see more information about expert reviewing. |
Error in widget FBRecommend: unable to write file /var/www/wikivet.net/extensions/Widgets/compiled_templates/wrt674397f9126953_62927151 Error in widget google+: unable to write file /var/www/wikivet.net/extensions/Widgets/compiled_templates/wrt674397f95e09b3_01186601 Error in widget TwitterTweet: unable to write file /var/www/wikivet.net/extensions/Widgets/compiled_templates/wrt674397f9a4a5e0_90449755
|
WikiVet® Introduction - Help WikiVet - Report a Problem |