Hepatic Encephalopathy - Horse
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.
No age, sex or breed predispositions.
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 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
A liver biopsy can provide a definitive diagnosis of liver disease; a clotting profile should be carried out before taking an ultrasound-guided biopsy.
Transabodimal ultrasound can be used to assess the structure of the liver and degree of damage.
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 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|
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|Hepatic Encephalopathy in horses publications|
- 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.
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