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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
- 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.