Neurological dysfunction in dogs following attenuation of congenital extrahepatic portosystemic shunts

Eleven of 89 dogs (12 per cent) developed neurological signs within six day s of surgical attenuation of a congenital extrahepatic portosystemic shunt. Neurological signs were not associated with hepatic encephalopathy or hypo glycaemia. Signs varied in severity from non-progressive ataxia (three dogs ) to generalised motor seizures (four dogs), progressing to status epilepti cus (three dogs), In a further four cases, ataxia and disorientation were t reated vigorously with anticonvulsant medication, presumably preventing the development of seizures. Two dogs that developed status epilepticus died o r were eventually euthanased. All other animals survived, although some had persistent neurological deficits. Postligation neurological complications were not prevented by gradual shunt attenuation. Prophylactic treatment wit h phenobarbitone (5 to 10 mg/kg preoperatively, followed by 3 to 5 mg/kg ev ery 12 hours for three weeks) did not significantly reduce the incidence of neurological sequelae (2/31 [6 per cent] dogs with phenobarbitone vs 9/58 [16 per cent] without phenobarbitone; P = 0.2). However, no animal receivin g phenobarbitone experienced generalised motor seizures or status epileptic us. In conclusion, these observations suggest that postligation neurologica l syndrome comprises a spectrum of neurological signs of variable severity Perioperative treatment with phenobarbitone may not reduce the risk of neur ological sequelae, but may reduce their severity.