Difference between revisions of "Hepatic Encephalopathy - Horse"

Revision as of 13:39, 19 August 2010

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 rae atypical but may occur in late stages of the syndrome.

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 fequently.

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
Rose, R. J. and Hodgson, D. R. (2000) Manual of Equine Practice (Second Edition) Sauders.

@@ Line 1: / Line 1: @@
-{{OpenPagesTop}}
+{{unfinished}}
-==Introduction==
+==Description==
-'''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.
+'''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.
-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.
+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 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.
+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 exaggerated.
+* 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 rae atypical but may occur in late stages of the syndrome.
 Additional clinical signs associated with hepatic disease:
@@ Line 31: / Line 28: @@
 ===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.
+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===
@@ Line 37: / Line 34: @@
 ===Pathology===
-See [[Hepatic Encephalopathy#Pathology|hepatic encephalopathy 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.
+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.
+'''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 fequently.
-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.
+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 of hepatic dysfunction. However with appropriate supportive therapy 40% of horses survive for at least 6 months. Recovery may be incomplete and temporary.
+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.
-{{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==
@@ Line 62: / Line 53: @@
 * 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.
+[[Category:To_Do_-_lizzyk]]
-{{review}}
+[[Category:Liver_Disorders_-_Horse]]
+[[Category:Neurological_Disorders_-_Horse]]
-{{OpenPages}}
-[[category:Expert_Review]]
-[[Category:Liver Diseases - Horse]]
-[[Category:Neurological Diseases - Horse]]