Hyperammonaemia in Dogs Presenting with Acute Epileptic Seizures—More than Portosystemic Shunts

Hyperammonaemia in dogs is most frequently associated with hepatic encephalopathy caused by portosystemic shunting. This retrospective multicentre study aimed to investigate the prevalence of hyperammonaemia and hepatic encephalopathy in dogs with recent or ongoing epileptic seizures. Furthermore, we sought to evaluate if transient post-ictal hyperammonaemia as a sequela to seizure activity occurs, as reported in humans and recently in cats. The medical records of all dogs presented between 2014 and 2024 to ten AniCura Veterinary Hospitals in Sweden were retrospectively reviewed to obtain those with recent or ongoing epileptic seizures with concurrent analysis of ammonia. The records of 267 dogs were extracted for further review. Inclusion criteria included information regarding the description and characterisation of the seizures and the analysis of ammonia within 24 h after last reported seizure activity. Additionally, hepatic function tests were required in dogs with elevated ammonia. In total, 58 dogs fulfilled the inclusion criteria, and 10 of those dogs (17%) had hyperammonaemia. Three dogs had documented hepatopathy, and two of them had surgically corrected portosystemic shunts. In seven dogs, no definitive cause of hyperammonaemia could be established. Three of the seven dogs had no evidence of portosystemic shunts, and six had no laboratory evidence supporting acute liver failure. According to the findings in this retrospective study, hyperammonaemia in the absence of evident acute hepatic failure or portosystemic shunting can occur in dogs with epileptic seizures, indicating that other differentials than hepatic encephalopathy should be considered. This study could not confirm the hypothesis of hyperammonaemia being a transient consequence of seizures.