Introduction
- Signs : alteration in behavior (sometimes profound), eg head pressing, disorientation, seizures, ataxia and collapse, and depression. Episodes may be related to feeding.
- Cause : exact cause is unknown but results from the liver being unable to remove toxic products of gut metabolism and to synthesize factors necessary for normal brain function.
- Underlying disorders: congenital portosystemic shunts
, urea cycle enzyme deficiencies, or acquired portosystemic shunts secondary to other hepatic disease, eg severe parenchymal liver damage due to cirrhosis, neoplasia, drugs, infection or toxins. - Diagnosis : demonstration of hepatic dysfunction and response to treatment.
- Treatment : fluid therapy, surgery, diet change, medical therapy, eg antibiotics, lactulose, 10% betadine solution enemas, emergency if in hepatic coma.
- Prognosis : good to fair.
Diagnosis
Clinical signs
- Disorientation.
- Head pressing.
- Blindness.
- Seizures.
- Ataxia.
- Collapse.
- Behavior change.
- Hepatic coma.
Diagnosis
Differential diagnosis
Sequelae
Prognosis
End stage hepatic cirrhosis- Poor even with proper dietary therapy and medical management.
- Good for full recovery if treated in early stages, ie not in hepatic coma with edema.
- Residual neurological defects may persist for long periods after recovery from hepatic coma.
- Dogs most commonly die post shunt ligation due to post surgical status epilepticus.
- Surgical ligation of shunts more likely to be successful if diagnosis and treated before cirrhosis or age.
Expected response to treatment
- A substantial decrease in, to total reversal of, neurological signs.
Reasons for treatment failure
- Incorrect diagnosis.
- General anesthetic complications.
- Portal hypertension.
- Post-surgical status epilepticus.
Sources
Publications
Refereed papers
- Recent references from PubMed.
- Mai W, Weisse C (2011) Contrast-enhanced portal magnetic resonance angioraphy in dogs with suspected congenital portal vascular anomalies. Vet Radiol Ultrasound 52, 284-288 PubMed.
- Gommeren K, Claeys S, de Rooster H, Haide A, Daminet S (2010) Outcome from status epilepticus after portosystemic shunt attentuation in 3 dogs with propofol and phenobarbital. J Vet Emerg Crit Care 20 , 346-351 PubMed.
- Greenhalgh S N, Dnuning M D, McKinley T J, Goodfellow M R, Kelman K R, Freitag T, O'Neill E J, Hall E J, Watson P J, Jeffrey N D (2010) Comparison of survival after surgical or medical treatment in dogs with a congenital portosystemic shunt. JAVMA 236 , 1215-1220 PubMed.
- Ruland K, Fischer A, Hartmann K (2010) Sensitivity and specificity of fasting ammonia and serum bile acids in the diagnosis of portosystemic shunts in dogs and cats. Vet Clin Pathol 39, 57-64 PubMed.
- d'Anjou M A, Penninck D, Cornejo L, Pibarot P (2004) Ultrasonographic diagnosis of portosystemic shunting in dogs and cats. Vet Radiol Ultrasound 45 , 424-437 PubMed.
- Winkler J T et al(2003) Portosystemic shunts: diagnosis, prognosis, and treatment of 64 cases (1993-2001). JAAHA 39 , 169 PubMed.
- Watson P J, Herrtage M E (1998) Medical managment of congenital portosystemic shunts in 27 dogs - a retrospective study. JSAP 39 , 62 PubMed.
- Watson (1997) Decision making in the management of portosystemic shunts. In Practice 19 , 106-120.
- Cuddon P A (1996) Metabolic encephalopathies. Vet Clin Nor Am Intracranial Disease 24 (4), 893-923.
- Torboada & Dimski (1995) Hepatic encephalopathy; clinical signs, pathogenesis and treatment. VCNA 25 , 337-355.
- Maddison J E (1994) Hepatic encephalopathy in dogs and cats. Vet Int 6 , 37-43.
- Maddison J E (1992) Current concepts of hepatic encephalopathy. JVIM 6 , 341-343.
Other sources of information
- Tobias K M (2003) Portosystemic shunts and other hepatic vascular anomalies. In: Textbook of Small Animal Surgery.3rd edn, Slatter D (ed), Philadelphia, p 727.
- LaFlamme D P (2000) Nutritional management of liver disease. In: Current Veterinary Therapy XIII. Bonagura J (ed), W B Saunders, Philadelphia. pp 683-687.








